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Szczepańska-Sadowska, E.W. Cardiovascular Effects of Vasopressin and Oxytocin. Encyclopedia. Available online: https://encyclopedia.pub/entry/15829 (accessed on 25 June 2024).
Szczepańska-Sadowska EW. Cardiovascular Effects of Vasopressin and Oxytocin. Encyclopedia. Available at: https://encyclopedia.pub/entry/15829. Accessed June 25, 2024.
Szczepańska-Sadowska, Ewa W.a.. "Cardiovascular Effects of Vasopressin and Oxytocin" Encyclopedia, https://encyclopedia.pub/entry/15829 (accessed June 25, 2024).
Szczepańska-Sadowska, E.W. (2021, November 09). Cardiovascular Effects of Vasopressin and Oxytocin. In Encyclopedia. https://encyclopedia.pub/entry/15829
Szczepańska-Sadowska, Ewa W.a.. "Cardiovascular Effects of Vasopressin and Oxytocin." Encyclopedia. Web. 09 November, 2021.
Cardiovascular Effects of Vasopressin and Oxytocin
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Oxytocin (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2; OXY) and arginine vasopressin (Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2; AVP) are nonapeptides, differing only in two aminoacids.  The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors.

oxytocin vasopressin hypertension

1. Effects of Oxytocin on the Cardiovascular System

Information about the effects of oxytocin on the cardiovascular system has been provided by a number of experimental studies. Oxytocin receptors are present in the heart, in the vessels, and in the cardiovascular regions of the brain [1][2][3][4][5][6]. In the vascular endothelial cells of large vessels and cardiac microvessels, they co-localize with endothelial nitric oxide (NO) synthase (eNOS) [7]. In the estrogen-sensitive regions of the brain, such as the hypothalamus and the amygdala, the induction and transcription of OXTR are regulated by estrogens and depend on the stimulation of estrogen receptors (ER). Stimulation of ERα enhances induction of OXTR, while activation of ERβ helps to maintain the transcription of OXTR [8][9].
The majority of experimental findings indicate that the administration of oxytocin exerts a hypotensive effect and that the magnitude of this effect depends on its central and peripheral actions (Figure 1). In normotensive rats remaining at rest, ICV administration of OXY significantly decreases blood pressure, but does not influence the heart rate [10][11]. It has been shown that the subchronic (5 days) subcutaneous application of OXY increases the hypotensive action of clonidine, and this action is abolished by the blockade of alpha-2 receptors (α2R). The latter finding suggests the involvement of α-2 noradrenergic receptors in the hypotensive action of OXY [12]. In Sprague Dawley rats, OXTR mRNA was detected in the vena cava, the pulmonary vein, and the aorta. Its presence was associated with a high expression of ANP mRNA in the vena cava and the pulmonary vein. OXTR mRNA was also identified in the mesenteric arteries and the uterine arcuate arteries of female Sprague Dawley rats. The expression of OXTR mRNA was enhanced by estrogen in the aorta and the vena cava [13][14] and it is worth noting that oxytocin did not cause vasodilation of the systemic arteries. In contrast, in high concentrations, OXY elicited vasoconstriction, which was mediated by the stimulation of V1aR [14].
Figure 1. The role of oxytocin in cardiovascular regulation. Oxytocin stimulates specific receptors (OXTR) and vasopressin receptors (V1aR) in different organs. In the central nervous system, it regulates the activity of several groups of neurons and may exert either stimulatory or inhibitory effects, depending on the site of action. The predominant effects of the action of oxytocin in the central nervous system involve reduced activation of the sympathetic division of the autonomic nervous system and enhanced activation of the parasympathetic division of the autonomic nervous system. Abbreviations: AP—area postrema; MnPO—median preoptic nucleus; NTS—nucleus tractus solitarii; OVLT—organum vasculosum of the lamina terminalis; PVN—paraventricular nucleus; RVLM—rostral ventrolateral medulla; 3rd—third ventricle; 4th—fourth ventricle.
Transcripts of OXTR were demonstrated both in the atrial and ventricular sections of the heart. It has been shown that activation of the oxytocin receptors plays an essential role in the release of ANP in the heart [15]. In vitro observations on pluripotent P19 embryonic stem cells have shown that OXY induces differentiation of these cells into cardiomyocytes [16].
Extensive findings from animal-derived models indicate that oxytocin may play a beneficial role in the regulation of cardiovascular functions in hypertension. In particular, peripheral subcutaneous injections of OXY in SHR rats resulted in hypotension and caused greater diurnal and nocturnal reductions in blood pressure [17][18]. It appears that the beneficial effect of oxytocin on blood pressure develops during the early postnatal period [19][20]. The buffering role of oxytocin in the regulation of blood pressure in SHR is impaired and even reversed during exposure to an alarming stress [21][22]. SHR rats respond to the application of acute stress with greater increases in blood pressure than WKY rats and this difference is abolished by the chronic ICV administration of OXY [22]. Hypertension is associated with the altered expression of oxytocin in the central nervous system and the adrenal glands of SHR [23]. Reduced expression of OXTR was found in SHR in the NTS and the dorsal brain stem [24][25]. More recently, it was shown that oxytocin released by neurons projecting from the PVN to the dorsal motor nucleus of the vagus prevents the development of hypertension in rats chronically exposed to hypoxia/hypercapnia—an animal model of human hypertension associated with OSAS [26].
Some studies suggest the engagement of oxytocin in hypertension-induced cardiac remodeling. In particular, it has been found that the blockade of cardiac OXTR facilitates the development of fibrosis and causes a reduction in the LV ejection fraction in SHR rats [5]. SHR also manifests elevated levels of OXY and OXTR in the left ventricle of the heart [27].
The cardiac oxytocinergic system plays an essential role in cardiac remodeling and cardioprotection during cardiac ischemia and post-infarct heart failure [28][29][30][31][32][33][34][35]. In the isolated heart rat model, submitted to a one hour ischemia-reperfusion-perfusion procedure, the administration of oxytocin during the early reperfusion phase reduced the size of the myocardial infarct and increased the coronary blood flow. This was associated with a decreased production of reactive oxygen species (ROS), a reduced expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and reduced apoptosis, reduced arrhythmia, and reduced ventricular fibrillation [33][34][35][36]. In addition, OXY increased the phosphorylated Hsp27 protein level and the atrial natriuretic peptide level in the cardiac left ventricle [33]. It should be noted that the cardioprotective actions of OXY are mediated through OXTR activation. The infusion of oxytocin elevated cell death in siRNA-mediated knockout cells with reduced expression of OXTR via binding with vasopressin receptors [36]. Centrally administered OXY decreases both the pressor response and the tachycardic response after exposure to an alarming stress in rats with myocardial infarction, but not in the sham-operated controls [37].
In the rat model of heart failure induced by pressure overloading of the left ventricle lasting four weeks, chronic stimulation of PVN neurons in adult Sprague Dawley rats resulted in several beneficial effects, such as a decrease in blood pressure and heart rate, a reduction of cellular hypertrophy, a reduction of fibrosis, a reduction of IL-1β concentration, and an improvement of the LV function [38]. Gutkowska et al. showed that oxytocin may prevent the development of diabetic cardiomyopathy. A downregulation of OXY gene expression in the heart of the db/db mouse model of type 2 diabetes mellitus has been reported [39]. Male db/db mice respond with a higher expression of cardiac OXTR, a lower fasting blood glucose level, reduced body fat accumulation, reduced ROS production, reduced cardiomyocyte hypertrophy, reduced fibrosis, and reduced apoptosis to prolonged (12 weeks) administration of oxytocin [31][40]. However, chronic overstimulation of OXTR may result in opposite and highly detrimental effects. It has been shown that 14-week-old transgenic α-MHC-Oxtr mice overexpressing oxytocin receptors manifest significantly greater left ventricle end-diastolic volume, prominent cardiac fibrosis, and enhanced expression of pro-fibrogenic genes. There is also a higher mortality rate among transgenic α-MHC-Oxtr mice than among the wild-type control strain [41].
To date, little is known about the cardiovascular effects of OXY in humans and further studies are needed. In line with experimental findings, OXY and its analogue carbetocin exert hypotensive effects during delivery. Rosseland et al. reported marked hypotension and an increase in the stroke volume after OXY/carbetocin administration during cesarean section [42]. Furthermore, in another study, the intravenous infusion of OXY during cesarean section resulted in stenocardia, transient profound tachycardia, hypotension, and electrocardiographic signs of myocardial ischemia [43]. It is worth noting that intranasal OXY administration caused a short-term increase in heart-rate variability in healthy volunteers [44].

2. Effects of Vasopressin on the Cardiovascular System

Vasopressin regulates blood pressure, blood flow, and body fluid volume through actions mediated by receptors located on vasopressin sensitive cardiovascular neurons in the brain and in the spinal cord, and on AVP receptors in numerous peripheral organs [45][46][47][48][49][50][51][52][53][54][55][56][57][58] (Figure 2). All types of vasopressin receptors are engaged in these actions. The central pressor action of vasopressin is mediated mainly by V1aR located in the RVLM and the rostral ventral respiratory column [59][60][61].
Figure 2. The role of vasopressin in cardiovascular regulation. Vasopressin stimulates specific types of receptors (V1aR, V1bR, and V2R) in various organs. In the central nervous system, it regulates the activity of several groups of neurons and exerts either stimulatory or inhibitory effects, depending on the site of action. Consequently, the effects of activation of both divisions of the autonomic nervous system (sympathetic and parasympathetic) can be observed, depending on specific factors provoking activation of the vasopressinergic system. Abbreviations: AP—area postrema; MnPO—median preoptic nucleus; NTS—nucleus tractus solitarii; OVLT—organum vasculosum of the lamina terminalis; PVN—paraventricular nucleus; RVLM—rostral ventrolateral medulla; 3rd—third ventricle; 4th—fourth ventricle.
Stimulation of V1aR also plays an essential role in the vasoconstriction of systemic, coronary, and renal vessels [62][63][64][65]. However, stimulation of V1aR also causes vasodilation of the pulmonary arteries [66]. In the kidney, V1aR is present in the basolateral membranes of the thick ascending limbs of Henle’s loop (TAL) and the collecting ducts (CD), and in the juxtaglomerular apparatus [67][68]. Experiments on V1aR deficient mice (V1aR−/−) strongly suggest that activation of V1aR in the kidney plays an essential role in the stimulation of the RAS and in the activation of the V2R-AQP2 pathway. Elimination of V1aR in these mice resulted in polyuria and the diminution of renin-containing granular cells and the plasma renin level, as well as in the reduction of V2R expression in the collecting ducts [69][70]. Downregulation of V1a receptors is observed in the vascular smooth muscles in sepsis elicited by the application of lipopolysaccharide or proinflammatory cytokines, and this may account for the reduced responsiveness to vasopressin in septic shock [71].
V1bR is located mainly in the brain, the pituitary, the pancreas, and the kidneys [72][73][74]. In the brain, V1bR mediates the activation of the PVN presympathetic neurons by vasopressin [60][75]. They are also engaged in the stimulation of insulin release from the pancreatic islet cells, and the release of ACTH from the anterior pituitary [76][77]. Expression of V1b receptor mRNA in the anterior pituitary is mediated by glucocorticoids [76]. V1bR is located mainly in the inner medulla in the kidney. There is evidence that stimulation of renal V1bR can counterbalance the antidiuretic effect of vasopressin mediated by V2R [78]. It is likely that the counteractive effects of the stimulation of V1bR and V2 receptors by vasopressin may account for the potent natriuretic effect observed after the combined administration of insulin and vasopressin in rats [79].
Vasopressin has long been known as an antidiuretic hormone due to its water retaining action in the kidney, exerted by V2 receptors. In the renal tubules, V2R is located mainly in the collecting duct cells, where it is coupled to Gs proteins. The stimulation of V2R results in the activation of adenylate cyclase, the formation of cAMP, and the activation of protein kinase A (PKA). This leads to the fast activation of AQP2 molecules and their translocation from the cytoplasmic vesicles to the apical cellular membrane where they form water channels. The channels enable the shift of water from the tubules to the cells and subsequently to the basolateral membrane. PKA also intensifies the synthesis of AQP2 molecules [80][81][82]. Activation of V2R increases water permeability in the kidney and enhances the shift of urea and sodium. Acting on V2 receptors, AVP enhances the transcription of the epithelial sodium channels (ENaC) and urea transporters, and promotes the synthesis of renin [80][81][82][83][84]. Consequently, the stimulation of V2R reduces water and sodium excretion and their blockade results in diuresis and natriuresis. The effectiveness of these actions depends on the state of hydration of the body and the availability of other factors operating in the renal tubules, such as Ang II and aldosterone. Aldosterone cooperates with AVP in the regulation of sodium transport via the epithelial sodium channels in the distal portion of the nephron [85]. Experiments on rats with diabetes insipidus have shown that aldosterone reduces the expression of AQP2 in the inner stripe of the outer medulla and increases free water clearance and creatinine clearance, whereas the mineralocorticoid receptor antagonist, spironolactone, elevates AQP2 expression and decreases creatinine clearance [86]. The stimulation of V2 receptors causes their internalization and recycling. This recycling is associated with increased sensitivity of the collecting ducts to vasopressin. The process of recycling is intensified in cardiac failure induced by the ligation of the left anterior descending coronary artery and may account for increased sensitivity to the antidiuretic action of vasopressin in heart failure [87].
Although the kidney is the main target organ expressing V2R, studies exploring the expression of V2R mRNA and the functional consequences of V2R blockade have shown that these receptors may also play a role in the regulation of the gastrointestinal tract, the heart, and the brain [88][89][90][61][91]. Experiments on embryonic stem cells have shown that vasopressin contributes to cardiac differentiation and its action is accomplished by the stimulation of V2 receptors and NO synthesis [92].
The blockade of vasopressin receptors may exert beneficial effects in the treatment of various forms of cardiac failure. The application of antagonists selectively blocking V2 receptors in the rat induces a significant aquaphoric effect and improves hemodynamics [93]. Experiments on pigs with cardiac failure induced by rapid pacing showed that the systemic administration of the V1a receptor antagonist (SR49059) elicited beneficial effects illustrated by a reduction of the left ventricle dimension and peak wall stress, although it did not improve cardiac muscle contractility. The authors reported that the effectiveness of the treatment of heart failure was significantly greater after simultaneous application of V1aR and angiotensin II antagonists [94]. The altered expression of V1aR has been reported in rats with myocardial infarction and in rats exposed to chronic stress. The infarcted rats manifested a reduced V1aR mRNA expression in the preoptic, diencephalic, and mesocenphalopontine regions of the brain. In contrast, the expression of V1aR receptors was significantly elevated in the brain medulla and in the renal cortex of chronically stressed rats [95]. Taking into account the pressor effect of the stimulation of V1a receptors in the brain, it is likely that the downregulation of these receptors during the post-infarct state is a protective response, which is suppressed during stress. There is evidence that the stimulation of V1aR may reduce the cerebral blood flow during dehydration and that this response is associated with an increased production of ROS and can be effectively abolished by the blockade of V1aR [96].
The results from clinical observations are in line with the experimental data. Patients with heart failure manifest a significantly greater expression of V1aR in the left ventricle myocardium than subjects with non-failing hearts [97]. To date, the application of various types of V1aR and V2R antagonists in the treatment of heart failure has provided inconclusive results in human clinical trials [98][99][100]. Nonetheless, recent clinical guidelines on the diagnosis and the treatment of heart failure issued by the European Society of Cardiology indicate that tolvaptan, a selective V2R antagonist, can be considered for the treatment of heart failure patients with hyponatremia [101]. Recently, promising results have been obtained in a double-blind, randomized phase II AVANTI study following the effects of the application of pecavaptan, a dual V1a/V2 antagonist in patients with heart failure and fluid overload. This study revealed that treatment with pecavaptan significantly enhances decongestion of the heart and improves the maintenance of the body fluid balance in patients with acute heart failure [102].

References

  1. Jankowski, M.; Hajjar, F.; Kawas, S.A.; Mukaddam-Daher, S.; Hoffman, G.; McCann, S.M.; Gutkowska, J. Rat heart: A site of oxytocin production and action. Proc. Natl. Acad. Sci. USA 1998, 95, 14558–14563.
  2. Jurek, B.; Neumann, I.D. The Oxytocin Receptor: From Intracellular Signaling to Behavior. Physiol. Rev. 2018, 98, 1805–1908.
  3. Gimpl, G.; Reitz, J.; Brauer, S.; Trossen, C. Oxytocin receptors: Ligand binding, signalling and cholesterol dependence. Prog. Brain Res. 2008, 170, 193–204.
  4. Gutkowska, J.; Jankowski, M. Oxytocin revisited: It is also a cardiovascular hormone. J. Am. Soc. Hypertens. 2008, 2, 318–325.
  5. Jankowski, M.; Bissonauth, V.; Gaom, L.; Gangal, M.; Wang, D.; Danalache, B.; Wang, Y.; Stoyanova, E.; Cloutier, G.; Blaise, G.; et al. Anti-inflammatory effect of oxytocin in rat myocardial infarction. Basic. Res. Cardiol. 2010, 105, 205–218.
  6. Sofroniew, M.V. Vasopressin and oxytocin in the mammalian brain and spinal cord. Trends Neurosci. 1983, 6, 467–472.
  7. Thibonnier, M.; Conarty, D.M.; Preston, J.A.; Plesnicher, C.L.; Dweik, R.A.; Erzurum, S.C. Human vascular endothelial cells express oxytocin receptors. Endocrinology 1999, 140, 1301–1309.
  8. Nomura, M.; McKenna, E.; Korach, K.S.; Pfaff, D.W.; Ogawa, S. Estrogen receptor-beta regulates transcript levels for oxytocin and arginine vasopressin in the hypothalamic paraventricular nucleus of male mice. Brain Res. Mol. Brain Res. 2002, 109, 84–94.
  9. Young, L.J.; Wang, Z.; Donaldson, R.; Rissman, E.F. Estrogen receptor alpha is essential for induction of oxytocin receptor by estrogen. Neuroreport 1998, 9, 933–936.
  10. Petersson, M.; Uvnäs-Moberg, K. Effects of an acute stressor on blood pressure and heart rate in rats pretreated with intracerebroventricular oxytocin injections. Psychoneuroendocrinology 2007, 32, 959–965.
  11. Petersson, M.; Alster, P.; Lundeberg, T.; Uvnäs-Moberg, K. Oxytocin causes a long-term decrease of blood pressure in female and male rats. Physiol. Behav. 1996, 60, 1311–1315.
  12. Petersson, M.; Lundeberg, T.; Uvnäs-Moberg, K. Oxytocin enhances the effects of clonidine on blood pressure and locomotor activity in rats. J. Auton. Nerv. Syst. 1999, 78, 49–56.
  13. Jankowski, M.; Wang, D.; Hajjar, F.; Mukaddam-Daher, S.; McCann, S.M.; Gutkowska, J. Oxytocin and its receptors are synthesized in the rat vasculature. Proc. Natl. Acad. Sci. USA 2000, 97, 6207–6211.
  14. Miller, M.E.; Davidge, S.T.; Mitchell, B.F. Oxytocin does not directly affect vascular tone in vessels from nonpregnant and pregnant rats. Am. J. Physiol. Heart Circ. Physiol. 2002, 282, H1223–H1228.
  15. Gutkowska, J.; Jankowski, M.; Lambert, C.; Mukaddam-Daher, S.; Zingg, H.H.; McCann, S.M. Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart. Proc. Natl. Acad. Sci. USA 1997, 94, 11704–11709.
  16. Paquin, J.; Danalache, B.A.; Jankowski, M.; McCann, S.M.; Gutkowska, J. Oxytocin induces differentiation of P19 embryonic stem cells to cardiomyocytes. Proc. Natl. Acad. Sci. USA 2002, 99, 9550–9555.
  17. Gutkowska, J.; Aliou, Y.; Lavoie, J.L.; Gaab, K.; Jankowski, M.; Broderick, T.L. Oxytocin decreases diurnal and nocturnal arterial blood pressure in the conscious unrestrained spontaneously hypertensive rat. Pathophysiology 2016, 23, 111–121.
  18. Petersson, M.; Lundeberg, T.; Uvnäs-Moberg, K. Oxytocin decreases blood pressure in male but not in female spontaneously hypertensive rats. J. Auton. Nerv. Syst. 1997, 66, 15–18.
  19. Holst, S.; Uvnäs-Moberg, K.; Petersson, M. Postnatal oxytocin treatment and postnatal stroking of rats reduce blood pressure in adulthood. Auton. Neurosci. 2002, 99, 85–90.
  20. Petersson, M.; Uvnäs-Moberg, K. Postnatal oxytocin treatment of spontaneously hypertensive male rats decreases blood pressure and body weight in adulthood. Neurosci. Lett. 2008, 440, 166–169.
  21. Wsol, A.; Szczepanska-Sadowska, E.; Kowalewski, S.; Puchalska, L.; Cudnoch-Jedrzejewska, A. Oxytocin differently regulates pressor responses to stress in WKY and SHR rats: The role of central oxytocin and V1a receptors. Stress 2014, 17, 117–125.
  22. Wsol, A.; Wojno, O.; Puchalska, L.; Wrzesien, R.; Szczepanska-Sadowska, E.; Cudnoch-Jedrzejewska, A. Impaired hypotensive effects of centrally acting oxytocin in SHR and WKY rats exposed to chronic mild stress. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2020, 318, R160–R172.
  23. Gaida, W.; Lang, R.E.; Kraft, K.; Unger, T.; Ganten, D. Altered neuropeptide concentrations in spontaneously hypertensive rats: Cause or consequence? Clin. Sci. (Lond.) 1985, 68, 35–43.
  24. Higa-Taniguchi, K.T.; Felix, J.V.; Michelini, L.C. Brainstem oxytocinergic modulation of heart rate control in rats: Effects of hypertension and exercise training. Exp. Physiol. 2009, 94, 1103–1113.
  25. Martins, A.S.; Crescenzi, A.; Stern, J.E.; Bordin, S.; Michelini, L.C. Hypertension and exercise training differentially affect oxytocin and oxytocin receptor expression in the brain. Hypertension 2005, 46, 1004–1009.
  26. Jameson, H.; Bateman, R.; Byrne, P.; Dyavanapalli, J.; Wang, X.; Jain, V.; Mendelowitz, D. Oxytocin neuron activation prevents hypertension that occurs with chronic intermittent hypoxia/hypercapnia in rats. Am. J. Physiol. Heart Circ. Physiol. 2016, 310, H1549–H1557.
  27. Wsol, A.; Gondek, A.; Podobinska, M.; Chmielewski, M.; Sajdel-Sułkowska, E.; Cudnoch-Jędrzejewska, A. Increased oxytocinergic system activity in the cardiac muscle in spontaneously hypertensive SHR rats. Arch. Med. Sci. 2019, 2019, 85446.
  28. Indrambarya, T.; Boyd, J.H.; Wang, Y.; McConechy, M.; Walley, K.R. Low-dose vasopressin infusion results in increased mortality and cardiac dysfunction following ischemia-reperfusion injury in mice. Crit. Care 2009, 13, R98.
  29. Faghihi, M.; Alizadeh, A.M.; Khori, V.; Latifpour, M.; Khodayari, S. The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart. Peptides 2012, 37, 314–319.
  30. Jankowski, M.; Wang, D.; Danalache, B.; Gangal, M.; Gutkowska, J. Cardiac oxytocin receptor blockade stimulates adverse cardiac remodeling in ovariectomized spontaneously hypertensive rats. Am. J. Physiol. Heart Circ. Physiol. 2010, 299, H265–H274.
  31. Jankowski, M.; Broderick, T.L.; Gutkowska, J. Oxytocin and cardioprotection in diabetes and obesity. BMC Endocr. Disord. 2016, 16, 34.
  32. Jankowski, M.; Broderick, T.L.; Gutkowska, J. The Role of Oxytocin in Cardiovascular Protection. Front. Psychol. 2020, 11, 2139.
  33. Ondrejcakova, M.; Barancik, M.; Bartekova, M.; Ravingerova, T.; Jezova, D. Prolonged oxytocin treatment in rats affects intracellular signaling and induces myocardial protection against infarction. Gen. Physiol. Biophys. 2012, 31, 261–270.
  34. Polshekan, M.; Jamialahmadi, K.; Khori, V.; Alizadeh, A.M.; Saeidi, M.; Ghayour-Mobarhan, M.; Jand, Y.; Ghahremani, M.H.; Yazdani, Y. RISK pathway is involved in oxytocin postconditioning in isolated rat heart. Peptides 2016, 86, 55–62.
  35. Polshekan, M.; Khori, V.; Alizadeh, A.M.; Ghayour-Mobarhan, M.; Saeidi, M.; Jand, Y.; Rajaei, M.; Farnoosh, G.; Jamialahmadi, K. The SAFE pathway is involved in the postconditioning mechanism of oxytocin in isolated rat heart. Peptides 2019, 111, 142–151.
  36. Gonzalez-Reyes, A.; Menaouar, A.; Yip, D.; Danalache, B.; Plante, E.; Noiseux, N.; Gutkowska, J.; Jankowski, M. Molecular mechanisms underlying oxytocin-induced cardiomyocyte protection from simulated ischemia-reperfusion. Mol. Cell Endocrinol. 2015, 412, 170–181.
  37. Wsol, A.; Cudnoch-Jedrzejewska, A.; Szczepanska-Sadowska, E.; Kowalewski, S.; Dobruch, J. Central oxytocin modulation of acute stress-induced cardiovascular responses after myocardial infarction in the rat. Stress 2009, 12, 517–525.
  38. Garrott, K.; Dyavanapalli, J.; Cauley, E.; Dwyer, M.K.; Kuzmiak-Glancy, S.; Wang, X.; Mendelowitz, D.; Kay, M.W. Chronic activation of hypothalamic oxytocin neurons improves cardiac function during left ventricular hypertrophy-induced heart failure. Cardiovasc. Res. 2017, 113, 1318–1328.
  39. Gutkowska, J.; Broderick, T.L.; Bogdan, D.; Wang, D.; Lavoie, J.M.; Jankowski, M. Downregulation of oxytocin and natriuretic peptides in diabetes: Possible implications in cardiomyopathy. J. Physiol. 2009, 587 Pt 19, 4725–4736.
  40. Plante, E.; Menaouar, A.; Danalache, B.A.; Yip, D.; Broderick, T.L.; Chiasson, J.L.; Jankowski, M.; Gutkowska, J. Oxytocin treatment prevents the cardiomyopathy observed in obese diabetic male db/db mice. Endocrinology 2015, 156, 1416–1428.
  41. Jung, C.; Wernly, B.; Bjursell, M.; Wiseman, J.; Admyre, T.; Wikström, J.; Palmér, M.; Seeliger, F.; Lichtenauer, M.; Franz, M.; et al. Cardiac-Specific Overexpression of Oxytocin Receptor Leads to Cardiomyopathy in Mice. J. Card Fail. 2018, 24, 470–478.
  42. Rosseland, L.A.; Hauge, T.H.; Grindheim, G.; Stubhaug, A.; Langesæter, E. Changes in blood pressure and cardiac output during cesarean delivery: The effects of oxytocin and carbetocin compared with placebo. Anesthesiology 2013, 119, 541–551.
  43. Svanström, M.C.; Biber, B.; Hanes, M.; Johansson, G.; Näslund, U.; Bålfors, E.M. Signs of myocardial ischaemia after injection of oxytocin: A randomized double-blind comparison of oxytocin and methylergometrine during Caesarean section. Br. J. Anaesth. 2008, 100, 683–689.
  44. Kemp, A.H.; Quintana, D.S.; Kuhnert, R.L.; Griffiths, K.; Hickie, I.B.; Guastella, A.J. Oxytocin increases heart rate variability in humans at rest: Implications for social approach-related motivation and capacity for social engagement. PLoS ONE 2012, 7, e44014.
  45. Murphy, D.; Konopacka, A.; Hindmarch, C.; Paton, J.F.; Sweedler, J.V.; Gillette, M.U.; Ueta, Y.; Grinevich, V.; Lozic, M.; Japundzic-Zigon, N. The hypothalamic-neurohypophyseal system: From genome to physiology. J. Neuroendocrinol. 2012, 24, 539–553.
  46. Thibonnier, M.; Graves, M.K.; Wagner, M.S.; Auzan, C.; Clauser, E.; Willard, H.F. Structure, sequence, expression, and chromosomal localization of the human V1a vasopressin receptor gene. Genomics 1996, 31, 327–334.
  47. Lolait, S.J.; O’Carroll, A.M.; Mahan, L.C.; Felder, C.C.; Button, D.C.; Young, W.S., 3rd; Mezey, E.; Brownstein, M.J. Extrapituitary expression of the rat V1b vasopressin receptor gene. Proc. Natl. Acad. Sci. USA 1995, 92, 6783–6787.
  48. Gutkowska, J.; Miskurka, M.; Danalache, B.; Gassanov, N.; Wang, D.; Jankowski, M. Functional arginine vasopressin system in early heart maturation. Am. J. Physiol. Heart Circ. Physiol. 2007, 293, H2262–H2270.
  49. Antunes-Rodrigues, J.; Ruginsk, S.G.; Mecawi, A.S.; Margatho, L.O.; Cruz, J.C.; Vilhena-Franco, T.; Reis, W.L.; Ventura, R.R.; Reis, L.C.; Vivas, L.M.; et al. Mapping and signaling of neural pathways involved in the regulation of hydromineral homeostasis. Braz. J. Med. Biol. Res. 2013, 46, 327–338.
  50. Szczepańska-Sadowska, E.; Simon-Oppermann, C.; Gray, D.; Simon, E. Control of central release of vasopressin. J. Physiol. (Paris) 1984, 79, 432–439.
  51. Szczepańska-Sadowska, E.; Simon-Oppermann, C.; Gray, D.A.; Simon, E. Plasma and cerebrospinal fluid vasopressin and osmolality in relation to thirst. Pflugers. Arch. 1984, 400, 294–299.
  52. Japundžić-Žigon, N.; Lozić, M.; Šarenac, O.; Murphy, D. Vasopressin & Oxytocin in Control of the Cardiovascular System: An Updated Review. Curr. Neuropharmacol. 2020, 18, 14–33.
  53. Cowley, A.W., Jr.; Cushman, W.C.; Quillen, E.W., Jr.; Skelton, M.M.; Langford, H.G. Vasopressin elevation in essential hypertension and increased responsiveness to sodium intake. Hypertension 1981, 3, I93–I100.
  54. Cowley, A.W., Jr.; Szczepanska-Sadowska, E.; Stepniakowski, K.; Mattson, D. Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension. Am. J. Physiol. 1994, 267 Pt 2, H751–H756.
  55. Góźdź, A.; Szczepańska-Sadowska, E.; Szczepańska, K.; Maśliński, W.; Luszczyk, B. Vasopressin V1a, V1b and V2 receptors mRNA in the kidney and heart of the renin transgenic TGR(mRen2)27 and Sprague Dawley rats. J. Physiol. Pharmacol. 2002, 53, 349–357.
  56. Gruber, C.W.; Koehbach, J.; Muttenthaler, M. Exploring bioactive peptides from natural sources for oxytocin and vasopressin drug discovery. Future Med. Chem. 2012, 4, 1791–1798.
  57. Guillon, G.; Trueba, M.; Joubert, D.; Grazzini, E.; Chouinard, L.; Côté, M.; Payet, M.D.; Manzoni, O.; Barberis, C.; Robert, M. Vasopressin stimulates steroid secretion in human adrenal glands: Comparison with angiotensin-II effect. Endocrinology 1995, 136, 1285–1295.
  58. Szczepanska-Sadowska, E.; Stepniakowski, K.; Skelton, M.M.; Cowley, A., Jr. Prolonged stimulation of intrarenal V1 vasopressin receptors results in sustained hypertension. Am. J. Physiol. 1994, 267, R1217–R1225.
  59. Kc, P.; Haxhiu, M.A.; Tolentino-Silva, F.P.; Wu, M.; Trouth, C.O.; Mack, S.O. Paraventricular vasopressin-containing neurons project to brain stem and spinal cord respiratory-related sites. Respir. Physiol. Neurobiol. 2002, 133, 75–88.
  60. Komnenov, D.; Quaal, H.; Rossi, N.F. V(1a) and V(1b) vasopressin receptors within the paraventricular nucleus contribute to hypertension in male rats exposed to chronic mild unpredictable stress. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2021, 320, R213–R225.
  61. Yang, Z.; Coote, J.H. The role of supraspinal vasopressin and glutamate neurones in an increase in renal sympathetic activity in response to mild haemorrhage in the rat. Exp. Physiol. 2006, 91, 791–797.
  62. Lankhuizen, I.M.; van Veghel, R.; Saxena, P.R.; Schoemaker, R.G. -vasopressin-induced responses on coronary and mesenteric arteries of rats with myocardial infarction: The effects of V1a- and V2-receptor antagonists. J. Cardiovasc. Pharmacol. 2000, 36, 38–44.
  63. Lankhuizen, I.M.; van Veghel, R.; Saxena, P.R.; Schoemaker, R.G. Vascular and renal effects of vasopressin and its antagonists in conscious rats with chronic myocardial infarction; evidence for receptor shift. Eur. J. Pharmacol. 2001, 423, 195–202.
  64. Sellke, N.; Kuczmarski, A.; Lawandy, I.; Cole, V.L.; Ehsan, A.; Singh, A.K.; Liu, Y.; Sellke, F.W.; Feng, J. Enhanced coronary arteriolar contraction to vasopressin in patients with diabetes after cardiac surgery. J. Thorac. Cardiovasc. Surg. 2018, 156, 2098–2107.
  65. Serradeil-Le Gal, C.; Villanova, G.; Boutin, M.; Maffrand, J.P.; Le Fur, G. Effects of SR 49059, a non-peptide antagonist of vasopressin V1a receptors, on vasopressin-induced coronary vasoconstriction in conscious rabbits. Fundam. Clin. Pharmacol. 1995, 9, 17–24.
  66. Walker, B.R.; Haynes, J.J.; Wang, H.L.; Voelkel, N.F. Vasopressin-induced pulmonary vasodilation in rats. Am. J. Physiol. 1989, 257, H415–H422.
  67. Izumi, Y.; Nakayama, Y.; Mori, T.; Miyazaki, H.; Inoue, H.; Kohda, Y.; Inoue, T.; Nonoguchi, H.; Tomita, K. Downregulation of vasopressin V2 receptor promoter activity via V1a receptor pathway. Am. J. Physiol. Renal. Physiol. 2007, 292, F1418–F1426.
  68. Terada, Y.; Tomita, K.; Nonoguchi, H.; Yang, T.; Marumo, F. Different localization and regulation of two types of vasopressin receptor messenger RNA in microdissected rat nephron segments using reverse transcription polymerase chain reaction. J. Clin. Investig. 1993, 92, 2339–2345.
  69. Aoyagi, T.; Koshimizu, T.A.; Tanoue, A. Vasopressin regulation of blood pressure and volume: Findings from V1a receptor-deficient mice. Kidney Int. 2009, 76, 1035–1039.
  70. Izumi, Y.; Hori, K.; Nakayama, Y.; Kimura, M.; Hasuike, Y.; Nanami, M.; Kohda, Y.; Otaki, Y.; Kuragano, T.; Obinata, M.; et al. Aldosterone requires vasopressin V1a receptors on intercalated cells to mediate acid-base homeostasis. J. Am. Soc. Nephrol. 2011, 22, 673–680.
  71. Bucher, M.; Hobbhahn, J.; Taeger, K.; Kurtz, A. Cytokine-mediated downregulation of vasopressin V(1A) receptors during acute endotoxemia in rats. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2002, 282, R979–R984.
  72. Lolait, S.J.; O’Carroll, A.M.; Brownstein, M.J. Molecular biology of vasopressin receptors. Ann. N. Y. Acad. Sci. 1995, 771, 273–292.
  73. Pena, A.; Murat, B.; Trueba, M.; Ventura, M.A.; Bertrand, G.; Cheng, L.L.; Stoev, S.; Szeto, H.H.; Wo, N.; Brossard, G.; et al. Pharmacological and physiological characterization of dvasopressin, the first V1b-selective agonist for rat vasopressin/oxytocin receptors. Endocrinology 2007, 148, 4136–4146.
  74. Saito, M.; Tahara, A.; Sugimoto, T.; Abe, K.; Furuichi, K. Evidence that atypical vasopressin V(2) receptor in inner medulla of kidney is V(1B) receptor. Eur. J. Pharmacol. 2000, 401, 289–296.
  75. El-Werfali, W.; Toomasian, C.; Maliszewska-Scislo, M.; Li, C.; Rossi, N.F. Haemodynamic and renal sympathetic responses to V1b vasopressin receptor activation within the paraventricular nucleus. Exp. Physiol. 2015, 100, 553–565.
  76. Aguilera, G.; Rabadan-Diehl, C. Regulation of vasopressin V1b receptors in the anterior pituitary gland of the rat. Exp. Physiol. 2000, 85, 19S–26S.
  77. Oshikawa, S.; Tanoue, A.; Koshimizu, T.A.; Kitagawa, Y.; Tsujimoto, G. Vasopressin stimulates insulin release from islet cells through V1b receptors: A combined pharmacological/knockout approach. Mol. Pharmacol. 2004, 65, 623–629.
  78. Hus-Citharel, A.; Bouby, N.; Corbani, M.; Mion, J.; Mendre, C.; Darusi, J.; Tomboly, C.; Trueba, M.; Serradeil-Le Gal, C.; Llorens-Cortes, C.; et al. Characterization of a functional V(1B) vasopressin receptor in the male rat kidney: Evidence for cross talk between V(1B) and V(2) receptor signaling pathways. Am. J. Physiol. Renal. Physiol. 2021, 321, F305–F321.
  79. Szczepanska-Sadowska, E.; Brzezinski, M. Interaction between effects of insulin and vasopressin on renal excretion of water and sodium in rats. Horm. Metab. Res. 1982, 14, 175–179.
  80. Ishikawa, S.E. Hyponatremia Associated with Heart Failure: Pathological Role of Vasopressin-Dependent Impaired Water Excretion. J. Clin. Med. 2015, 4, 933–947.
  81. Qian, Q. Salt, water and nephron: Mechanisms of action and link to hypertension and chronic kidney disease. Nephrology (Carlton) 2018, 23, 44–49.
  82. Robertson, G.L. The regulation of vasopressin function in health and disease. Recent Prog. Horm. Res. 1976, 33, 333–385.
  83. Gonzalez, A.A.; Cifuentes-Araneda, F.; Ibaceta-Gonzalez, C.; Gonzalez-Vergara, A.; Zamora, L.; Henriquez, R.; Rosales, C.B.; Navar, L.G.; Prieto, M.C. Vasopressin/V2 receptor stimulates renin synthesis in the collecting duct. Am. J. Physiol. Renal. Physiol. 2016, 310, F284–F293.
  84. Schrier, R.W. Vasopressin and aquaporin 2 in clinical disorders of water homeostasis. Semin Nephrol. 2008, 28, 289–296.
  85. Stockand, J.D. Vasopressin regulation of renal sodium excretion. Kidney Int. 2010, 78, 849–856.
  86. Nielsen, J.; Kwon, T.H.; Praetorius, J.; Frøkiaer, J.; Knepper, M.A.; Nielsen, S. Aldosterone increases urine production and decreases apical AQP2 expression in rats with diabetes insipidus. Am. J. Physiol. Renal. Physiol. 2006, 290, F438–F449.
  87. Brønd, L.; Müllertz, K.M.; Torp, M.; Nielsen, J.; Graebe, M.; Hadrup, N.; Nielsen, S.; Christensen, S.; Jonassen, T.E. Congestive heart failure in rats is associated with increased collecting duct vasopressin sensitivity and vasopressin type 2 receptor reexternalization. Am. J. Physiol. Renal. Physiol. 2013, 305, F1547–F1554.
  88. Monstein, H.J.; Truedsson, M.; Ryberg, A.; Ohlsson, B. Vasopressin receptor mRNA expression in the human gastrointestinal tract. Eur. Surg. Res. 2008, 40, 34–40.
  89. Juul, K.V.; Bichet, D.G.; Nielsen, S.; Nørgaard, J.P. The physiological and pathophysiological functions of renal and extrarenal vasopressin V2 receptors. Am. J. Physiol. Renal. Physiol. 2014, 306, F931–F940.
  90. Robertson, G.L. Differential diagnosis of familial diabetes insipidus. Handb. Clin. Neurol. 2021, 181, 239–248.
  91. Cowley, A.W., Jr. Control of the renal medullary circulation by vasopressin V1 and V2 receptors in the rat. Exp. Physiol. 2000, 85, 223S–231S.
  92. Gassanov, N.; Jankowski, M.; Danalache, B.; Wang, D.; Grygorczyk, R.; Hoppe, U.C.; Gutkowska, J. Arginine vasopressin-mediated cardiac differentiation: Insights into the role of its receptors and nitric oxide signaling. J. Biol. Chem. 2007, 282, 11255–11265.
  93. Burrell, L.M.; Phillips, P.A.; Stephenson, J.M.; Risvanis, J.; Johnston, C.I. Vasopressin and a nonpeptide antidiuretic hormone receptor antagonist (OPC-31260). Blood Press. 1994, 3, 137–141.
  94. Clair, M.J.; King, M.K.; Goldberg, A.T.; Hendrick, J.W.; Nisato, R.; Gay, D.M.; Morrison, A.E.; McElmurray, J.H., 3rd; Krombach, R.S.; Bond, B.R.; et al. Selective vasopressin, angiotensin II, or dual receptor blockade with developing congestive heart failure. J. Pharmacol. Exp. Ther. 2000, 293, 852–860.
  95. Milik, E.; Szczepanska-Sadowska, E.; Dobruch, J.; Cudnoch-Jedrzejewska, A.; Maslinski, W. Altered expression of V1a receptors mRNA in the brain and kidney after myocardial infarction and chronic stress. Neuropeptides 2014, 48, 257–266.
  96. Faraco, G.; Wijasa, T.S.; Park, L.; Moore, J.; Anrather, J.; Iadecola, C. Water deprivation induces neurovascular and cognitive dysfunction through vasopressin-induced oxidative stress. J. Cereb. Blood Flow Metab. 2014, 34, 852–860.
  97. Zhu, W.; Tilley, D.G.; Myers, V.D.; Tsai, E.J.; Feldman, A.M. Increased vasopressin 1A receptor expression in failing human hearts. J. Am. Coll. Cardiol. 2014, 63, 375–376.
  98. Gheorghiade, M.; Konstam, M.A.; Burnett, J.C., Jr.; Grinfeld, L.; Maggioni, A.P.; Swedberg, K.; Udelson, J.E.; Zannad, F.; Cook, T.; Ouyang, J.; et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: The EVEREST Clinical Status Trials. Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) Investigators. JAMA 2007, 297, 1332–1343.
  99. Udelson, J.E.; McGrew, F.A.; Flores, E.; Ibrahim, H.; Katz, S.; Koshkarian, G.; O’Brien, T.; Kronenberg, M.W.; Zimmer, C.; Orlandi, C.; et al. Multicenter, randomized, double-blind, placebo-controlled study on the effect of oral tolvaptan on left ventricular dilation and function in patients with heart failure and systolic dysfunction. J. Am. Coll. Cardiol. 2007, 49, 2151–2159.
  100. Urbach, J.; Goldsmith, S.R. Vasopressin antagonism in heart failure: A review of the hemodynamic studies and major clinical trials. Ther. Adv. Cardiovasc. Dis. 2021, 15, 1753944720977741.
  101. McDonagh, T.A.; Metra, M.; Adamo, M.; Gardner, R.S.; Baumbach, A.; Böhm, M.; Burri, H.; Butler, J.; Čelutkienė, J.; Chioncel, O.; et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur. Heart J. 2021, 42, 3599–3726.
  102. Goldsmith, S.R.; Burkhoff, D.; Gustafsson, F.; Voors, A.; Zannad, F.; Kolkhof, P.; Staedtler, G.; Colorado, P.; Dinh, W.; Udelson, J.E. Dual Vasopressin Receptor Antagonism to Improve Congestion in Patients With Acute Heart Failure: Design of the AVANTI Trial. J. Card Fail. 2021, 27, 233–241.
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