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PubMed1988

Lectin-gold labeling of glycoconjugates in normal and Brattleboro rat papilla: effect of vasopressin.

Some reports suggest that the plasma membrane glycocalyx of collecting duct epithelial cells, as well as interstitial glycoconjugates, may be involved in vasopressin action and urinary concentration. In view of this, we have used the lectin-gold technique to map and quantify Helix pomatia lectin (HPL)-binding sites in the inner medulla of kidneys from normal Long-Evans rats, vasopressin-deficient Brattleboro rats, and Brattleboro rats treated for up to 5 wk with exogenous vasopressin. The results show that the labeling of epithelial cell plasma membranes from collecting ducts and thin limbs of Henle is not different between normal and Brattleboro rats, and the labeling is not modified by chronic vasopressin treatment. In contrast, the heavy interstitial labeling seen in normal rats is virtually absent from Brattleboro rats, but it is progressively restored by chronic vasopressin treatment of Brattleboro rats. These results show that vasopressin does not modify HPL-binding glycoconjugates on epithelial cell plasma membranes, but that vasopressin treatment has a major effect on HPL-binding glycoconjugates in the medullary interstitium.

Animals↗
PubMed1991

Effects of vasopressin and cAMP on single amiloride-blockable Na channels.

To determine the mechanism by which vasopressin increases sodium transport in sodium-transporting, tight epithelia, we examined single amiloride-blockable Na channels in membrane patches from cultured distal nephron cells (A6) either before or after treatment with arginine vasopressin. Pretreatment of cells with vasopressin (40 mU/ml) for 40-50 min increases NPo (N, the number of Na channels; Po, the open probability of an individual Na channel). The increase in NPo is due to an increase in the number of conductive Na channels with little or no change in the open probability of individual Na channels. Pretreatment of cells for 1 h with 1 mM N6,2'-O-dibutyryladenosine 3', 5'-cyclic monophosphate (DBcAMP) also increased NPo. The increase in NPo caused by DBcAMP pretreatment is also due to the increase in the number of conductive Na channels with no change in the open probability of individual Na channels. Cells pretreated with cholera toxin (CTX; 250 ng/ml) for 4 h appeared similar to cells that had been treated with vasopressin or DBcAMP; that is, the number of Na channels per patch increased with little or no effect on the open probability of individual Na channels. For patches from many untreated cells, when the frequency of occurrence is plotted against the number of channels in an individual patch, the histogram consists of a single peak with a number of channels per patch of 2.0 +/- 1.5 (+/- SD, 126 patches). After pretreatment of cells with vasopressin, DBcAMP, or CTX, the same histogram contains two peaks after vasopressin of 1.8 +/- 1.2 and 9.2 +/- 1.5 (+/- SD, 38 and 53 patches, respectively). These observations suggest that pretreatment of cells with vasopressin, DBcAMP, or CTX may act by promoting insertion of clusters of new sodium channels.

Amiloride↗
PubMed1990

In vivo somatostatin, vasopressin, and oxytocin synthesis in diabetic rat hypothalamus.

The in vivo labeling of somatostatin-14, somatostatin-28, arginine vasopressin, and oxytocin was studied in rat hypothalamus after third ventricular administration of [35S]cysteine to streptozotocin-diabetic and normal rats. Immunoreactive somatostatin levels in hypothalamus were unaffected by diabetes, as was the incorporation of [35S]cysteine into hypothalamic somatostatin-14 and somatostatin-28. In contrast, immunoreactive vasopressin levels in hypothalamus and posterior pituitary (and oxytocin levels in posterior pituitary) were below normal in diabetic rats. Moreover, [35S]cysteine incorporation into hypothalamic vasopressin and oxytocin (probably mainly in the paraventricular nucleus because of its proximity to the third ventricular site of label injection) was significantly above normal. The increments in vasopressin and oxytocin labeling were reversed by insulin administration. In vivo cysteine specific activity and the labeling of acid-precipitable protein did not differ between normal and diabetic animals; effects of diabetes on vasopressin and oxytocin labeling were therefore not caused by simple differences in cysteine specific activity. These results suggest that diabetes 1) does not influence the production of somatostatin peptides in hypothalamus but 2) stimulates the synthesis of vasopressin and oxytocin. For vasopressin at least, the increase in synthesis may be a compensatory response to the known increase in its secretion that occurs in uncontrolled diabetes.

Animals↗
PubMed1988

Stimulation of taurocholate and glycocholate efflux from the rat hepatocyte by arginine vasopressin.

Vasopressin induces alterations in the transmembrane distribution of the bile salts taurocholate and glycocholate but not of cholate, chenodeoxycholate, or chenodeoxycholate derivatives in isolated rat hepatocytes in suspension. Studies were conducted to define the specific transport events modulated by vasopressin. Unidirectional uptake of cholate, taurocholate, and glycocholate, monitored within a 15-s time frame, is not altered by vasopressin. Km values for cholate, taurocholate, and glycocholate influx were found to be 57, 12, and 26 microM, respectively. Vmax values for influx of cholate, taurocholate, and glycocholate were 1.7, 1.8, and 2.4 nmol.mg protein-1.min-1, respectively. At half-maximal effective concentrations, arginine vasopressin increases unidirectional efflux of taurocholate by 34% (EC50 = 1.5 X 10(-9) M) and glycocholate by 17% (EC50 = 5 X 10(-9) M). In the presence of 0.05 microM arginine vasopressin, the apparent Km value for taurocholate efflux decreases from 1.57 mM (control) to 0.94 mM; for glycocholate, the apparent Km decreases from 5.19 mM (control) to 3.22 mM. Vasopressin does not significantly change the Vmax values for taurocholate and glycocholate efflux (0.40 and 1.05 nmol.mg protein-1.min-1, respectively). These studies suggest that modulation of bile salt efflux by vasopressin may be utilized to probe bile salt transport pathways in the rat hepatocyte.

Animals↗
PubMed1998

Gap junctional communication coordinates vasopressin-induced glycogenolysis in rat hepatocytes.

Because hepatocytes communicate via gap junctions, it has been proposed that Ca2+ waves propagate through this pathway and in the process activate Ca2+-dependent cellular responses. We testedthis hypothesis by measuring vasopressin-induced glycogenolysis in short-term cultures of rat hepatocytes. A 15-min vasopressin (10(-8) M) stimulation induced a reduction of glycogen content that reached a maximum 1-3 h later. Gap junction blockers, octanol or 18alpha-glycyrrhetinic acid, reduced the effect by 70%. The glycogenolytic response induced by Ca2+ ionophore 8-bromo-A-21387, which acts on each hepatocyte, was not affected by gap junction blockers. Moreover, the vasopressin-induced glycogenolysis was lower (70%) in dispersed than in reaggregated hepatocytes and in dispersed hepatocytes was not affected by gap junction blockers. In hepatocytes reaggregated in the presence of a synthetic peptide homologous to a domain of the extracellular loop 1 of the main hepatocyte gap junctional protein, vasopressin-induced glycogenolysis and incidence of dye coupling were drastically reduced. Moreover, gap junctional communication was detected between reaggregated cells, suggesting that hepatocytes with different vasopressin receptor densities become coupled to each other. The vasopressin-induced effect was not affected by suramin, ruling out ATP as a paracrine mediator. We propose that gap junctions allow for a coordinated vasopressin-induced glycogenolytic response despite the heterogeneity among hepatocytes.

Adenosine Triphosphate↗
PubMed1978

Vasopressin in the rat with spontaneous hypertension.

Because vasopressin is one of the most potent naturally occurring pressor agents, and because of its importance in the regulation of blood volume and composition, we have undertaken a study of the role of vasopressin in the pathogenesis of the hypertension in the Okamoto-Aoki spontaneously hypertension (SH) rat. In SH rats, systolic blood pressure increased from 135 +/- 3 (SE) mmHg at age 33 days to 184 +/- 3 mmHg at age 75 days (P less than 0.01). In the Wistar-Kyoto (WKY) control rats, blood pressure increased from 100 +/- 2 to 120 +/- 2 mmHg (P less than 0.01). The differences in blood pressure between the SH and WKY rats at all ages were significant (P less than 0.01). During the age period 33-75 days, the 24-h urinary excretion of vasopressin in the SH rat was consistently more than twofold greater (P less than 0.01) than in the WKY rat. Plasma vasopressin concentration and pituitary vasopressin content were also elevated in the SH rat (P less than 0.01 and P less than 0.02, respectively). Changes in systolic blood pressure in the SH rat, however, were not paralleled by changes in the urinary excretion of vasopressin. The data indicate that the secretion of vasopressin is elevated in the SH rat. However, the magnitude of this elevation, in and of itself, may not be sufficient to account for the rising blood pressure in the young SH rat.

Animals↗
PubMed1979

Hypophysectomy and saralasin on mesenteric vasoconstrictor response to vasopressin.

The dose-response relationship of the mesenteric resistance vessels to vasopressin was studied in anesthetized laparotomized cats before and after hypophysectomy and again during the plateau phase of the response to a prolonged infusion of [Sar1-Ala8] angiotensin II (saralasin), a competitive antagonist of angiotensin II. Hypophysectomy and saralasin each caused an increase in superior mesenteric arterial conductance. Before hypophysectomy infusion of 0.5 mU/(min.kg) of vasopressin caused mesenteric conductance to decrease from 0.168 to 0.156 ml/(min.kg.mmHg), a change of only 0.012 units. After hypophysectomy, the same dose reduced conductance from 0.227 to 0.179 mU/(min.kg.mmHg), a change of 0.048 units. During the plateau phase of the response to saralasin, 0.5 mU/(min.kg) of vasopressin reduced conductance from 0.281 to 0.201 ml/(min.kg.mmHg), a change of 0.079 units. Hypophysectomy and saralasin had little effect on the mesenteric vasoconstrictor response to high doses of vasopressin (2.0-10 mU/(min.kg). The ineffectiveness of low doses of vasopressin on the mesenteric resistance vessels of the intact anesthetized, surgically stressed animal may be due in part to the already constricted state of the bed caused by endogenous vasopressin and angiotensin and in part due to an opposing vasodilator influence, the reflex withdrawal of the vasoconstrictor effect of endogenous vasopressin.

Angiotensin II↗
PubMed1988

Carotid sinus pressure and plasma vasopressin in anesthetized rabbits.

The arterial baroreceptors are known to influence the release of vasopressin, but the quantitative relationship between baroreceptor stimulation and plasma vasopressin concentration has not been defined. These experiments examine the effect of stepwise changes in carotid sinus pressure (40-160 mmHg) on the plasma concentration of vasopressin in chloralose-urethan anesthetized rabbits. Plasma vasopressin concentration (9.2 +/- 1.2 pg/ml, n = 27) did not change in response to changes in carotid sinus pressure when the aortic depressor nerves were intact. These results were unaltered by bilateral cervical vagotomy. However, after aortic depressor nerve section, decreases in carotid sinus pressure were associated with increases in plasma vasopressin concentration. There appeared to be a greater redundancy in the baroreceptor control of plasma vasopressin than in the baroreceptor control of arterial pressure or heart rate. The results provided no evidence that receptors with vagal afferents have a tonic influence on the baroreceptor control of vasopressin release in the anesthetized rabbit.

Animals↗
PubMed1989

Effects of endothelin and vasopressin on cerebral blood vessels.

Endothelin is a recently described peptide which has been suggested to be one type of endothelium-derived contracting factor. The goals of the present study were to examine the effects of endothelin and vasopressin on diameter of cerebral vessels and on permeability of the blood-brain barrier to fluorescein sodium (mol wt of 376). In anesthetized rats, topical suffusion of arginine vasopressin (10(-10) to 10(-7) M) decreased the diameter of pial arterioles, with a reduction of 27 +/- 1% at 10(-7) M in cerebrum and 35 +/- 2% at 10(-8) M for the basilar artery. A low concentration of endothelin (10(-10) M) produced modest (5 +/- 1%) dilatation of pial arterioles. Higher concentrations of endothelin (10(-8) and 10(-7) M) constricted pial arterioles with a reduction in diameter of 22 +/- 5% at 10(-7) M. Dilatation to endothelin was not observed in the basilar artery. The basilar artery constricted to lower doses of vasopressin than endothelin, but vasoconstriction to 10(-7) M endothelin (56 +/- 4%) was greater (P less than 0.05) than that for the same dose of vasopressin. Permeability of the blood-brain barrier to fluorescein sodium was not increased by vasopressin or endothelin. Thus 1) vasopressin produces constriction of brain blood vessels; 2) endothelin produces dilatation of pial arterioles at low doses but constriction at high doses; 3) constrictor responses to both peptides appear to be greater in the brain stem than in the cerebrum; and 4) vasopressin and endothelin do not increase permeability of the blood-brain barrier.

Animals↗
PubMed1992

Prostanoids modulate opioid-induced increases in cerebrospinal fluid vasopressin concentration.

Topical dynorphin and beta-endorphin produce increases in both prostanoid and vasopressin concentrations in cortical periarachnoid fluid of newborn pigs. The present study, in anesthetized piglets with cranial windows implanted, investigated the role of these prostanoids in the mediation of this vasopressin release by opioids. Topical prostaglandin (PG) I2 (100 ng/ml) increased pial arteriolar diameter from 145 +/- 4 to 178 +/- 4 microns and also increased cerebrospinal fluid (CSF) vasopressin from 1.1 +/- 0.1 to 4.1 +/- 0.5 microU/ml, but CSF vasopressin was not changed by PGE2, PGF2 alpha, and U-46619. Therefore, it is possible that PGI2 causes the increase in CSF vasopressin produced by opioids. Consistent with this concept, indomethacin and aspirin blocked dynorphin- and beta-endorphin-induced vasopressin release. The present data indicate that PGI2 contributes to opioid-induced changes in CSF vasopressin concentration and, thereby, to vasopressinergic contributions to opioid-induced cerebral vascular responses.

Animals↗
PubMed1993

Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery.

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.

Animals↗
PubMed2006

Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats.

Cardiovascular deconditioning occurs in astronauts after spaceflight or in individuals subjected to bed rest. It is characterized by an increased incidence of orthostatic intolerance. The mechanisms responsible for orthostatic intolerance are likely multifactorial and may include hypovolemia, autonomic dysfunction, and vascular and cardiac alterations. The arterial baroreflex is an important compensatory mechanism in the response to an orthostatic stress. In a previous study, we demonstrated that arterial baroreflex mediated sympathoexcitation was blunted in hindlimb-unloaded (HU) rats, a model of cardiovascular deconditioning. The arterial baroreflex also contributes to the regulation of vasoactive hormones including vasopressin and angiotensin II. In the present study, we tested the hypothesis that the neurohumoral response to hypotension is also attenuated in rats after 14 days of hindlimb unloading. To test this hypothesis, the vasodilator diazoxide (15 or 25 mg/kg) or saline (0.9%) was administered to produce hypotension or control conditions, respectively, in conscious HU and control rats. Plasma samples were collected and assayed for vasopressin and plasma renin activity (PRA). Diazoxide (25 mg/kg) produced significant increases in vasopressin and PRA compared with saline controls. HU rats exhibited significantly higher levels of vasopressin at rest and the increase in vasopressin levels during hypotension was enhanced by hindlimb unloading. Neither resting nor hypotension-induced PRA was altered by hindlimb unloading. These data suggest that although baroreflex-mediated sympathoexcitation is blunted by hindlimb unloading, hypotension-induced vasopressin release is enhanced and hypotension-induced PRA is unaffected. Increased circulating vasopressin may serve to compensate for blunted baroreflex regulation of sympathetic nervous activity produced by hindlimb unloading or may actually contribute to it.

Animals↗
PubMed1985

Acute reduction of plasma vasopressin levels by rehydration in sheep.

Sheep were depleted of water by restricting water intake to 500 ml/day for 7-9 days and were then rehydrated by three treatments: voluntary intake of water, administration of water by tube into the stomach, or voluntary intake of 0.9% NaCl solution (saline). The volumes of fluids drunk within 2-3 min, or administered by tube, were approximately equal to the animal's weight loss. Plasma vasopressin rose from 4.4 +/- 0.6 to 16.8 +/- 1.0 pg/ml during water restriction. After drinking water plasma vasopressin fell from 19.0 +/- 1.9 to 7.5 +/- 0.4 pg/ml (P less than 0.001) in 15 min and gradually fell to 3.2 +/- 0.4 pg/ml over 6 h. Plasma osmolality fell from 302.4 +/- 0.9 to 301.0 +/- 1.1 mosmol/kg (NS) 15 min after water drinking and then gradually fell to subnormal levels. Sheep given water by stomach tube showed a similar decline in plasma osmolality, but the fall in plasma vasopressin was attenuated. The fall in plasma vasopressin in the first 30 min after drinking saline was almost identical with the fall after drinking water, but plasma osmolality was unaltered. Plasma vasopressin fell so rapidly after drinking water or saline as to suggest that the act of drinking caused almost complete inhibition of vasopressin release without a change in plasma osmolality. The results are consistent with earlier evidence that oropharyngeal receptors initiate the inhibition of vasopressin release after drinking.

Animals↗
PubMed1985

Hemorrhage in DOC-salt hypertensive rats: plasma and platelet vasopressin.

The effect of two consecutive hemorrhages, each 10% of blood volume, on plasma vasopressin concentrations was determined in conscious unilaterally nephrectomized Long-Evans rats made hypertensive by treatment for 3 wk with deoxycorticosterone (DOC) and substitution of 1% saline for drinking water (DOC-salt rats) or DOC alone (DOC rats) and in normotensive unilaterally nephrectomized rats drinking water (H2O rats) or saline (NaCl rats). In response to 20% hemorrhage, blood pressure decreased more (P less than 0.01) and plasma vasopressin increased less (P less than 0.01) in the DOC-salt rats than in the other groups. Under basal conditions, immunoreactive vasopressin was found in the platelets in NaCl, DOC, and DOC-salt rats (P less than 0.01) but not in H2O rats. Platelet vasopressin increased (P less than 0.05-0.01) in response to hemorrhage only in DOC-salt rats. In conclusion, the vasopressin response to hemorrhage in DOC-salt rats is impaired; platelet immunoreactive vasopressin is of little importance in normal rats but is increased by treatment with DOC and/or chronic salt loading; and platelet vasopressin increased in response to hemorrhage only in DOC-salt rats.

Animals↗
PubMed1986

Osmoregulation during high salt intake: relative importance of drinking and vasopressin secretion.

Studies determined the relative contribution of drinking vs. vasopressin secretion in the regulation of extracellular osmolality in response to changes of Na intake. Daily Na intake was increased from 30 to 200 meq in dogs maintained under three conditions: normal dogs with ad libitum drinking, normal dogs with "fixed drinking," and neurohypophysectomized dogs with "fixed drinking" and vasopressin replaced by continuous infusion. (Drinking was fixed to that amount consumed during the normal Na control period.) The mechanisms of osmoregulation were highly nonlinear. As daily Na intake increased from 30 to 100 meq, renal natriuretic mechanisms predominated with only small contributions from either the thirst or vasopressin systems. At high levels of Na intake (200 meq/day), both drinking and vasopressin release contributed significantly to osmoregulation. The studies also determined that, in the absence of excess vasopressin secretion and increased drinking, plasma osmolality rose to nearly twice the levels as those observed in normal dogs that increased vasopressin secretion. We conclude that vasopressin-related renal conservation of water contributes to buffering the rise of osmolality when Na intake is increased without increased drinking. The studies also confirm that with available water to drink, the thirst mechanism together with renal Na excretory mechanisms are the predominant controllers of osmolality in situations of high sodium intake.

Animals↗
PubMed1988

Ventricular receptors stimulate vasopressin release during hemorrhage.

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.

Aldosterone↗
PubMed1988

Osmoregulation of thirst and vasopressin during normal menstrual cycle.

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

Adult↗
PubMed1988

Pressor responsiveness to and secretion of vasopressin during the estrous cycle.

Previously, we observed a sexual dimorphism of the pressor responsiveness to vasopressin in the rat. We have now determined that the pressor action of vasopressin is influenced by the phase of the estrous cycle. Conscious unrestrained male and female rats were given graded intravenous 30-min infusions of vasopressin. The pressor responses of male and estrous female rats were similar, whereas the pressor responses of diestrous, proestrous, and metestrous females were substantially (P less than 0.01) attenuated. This effect could not be attributed to differences in baroreflex sensitivity, which was unaffected by the sex of the rat or phase of the estrous cycle. Baroreflex sensitivity was assessed by the slope of the relationship between changes in heart rate and mean arterial blood pressure in response to graded injections of phenylephrine and nitroprusside. The basal plasma vasopressin concentration was higher (P less than 0.05) in male than in female rats in each phase of the estrous cycle. This was due to a difference in vasopressin release, since there were no sex-related differences in the metabolic clearance rate of vasopressin. These findings suggest that the gonadal hormones influence the cardiovascular actions of vasopressin and its secretion.

Angiotensin II↗