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PubMed2005

BSC1 inhibition complements effects of vasopressin V2 receptor antagonist on hyponatremia in SIADH rats.

BACKGROUND: Severe hyponatremia is most frequently caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Although the expressional alteration of the kidney-specific apical water channel, aquaporin 2 (AQP2), in the collecting duct has been demonstrated to be involved in the development of hyponatremia and the subsequent physiologic reaction that is resistant to arginine vasopressin (AVP; vasopressin escape) in SIADH, the complete pathogenesis of and the appropriate medical treatment for hyponatremia have yet to be elucidated. METHODS: Hyponatremia was induced in male Sprague-Dawley rats by water loading and subcutaneous infusion of 1-deamino-8-D-arginine vasopressin (dDAVP). For the treatment, a selective AVP V(2) receptor antagonist (OPC-31260) and/or a loop diuretic (furosemide) were administered orally. Protein expression of AQP2 and rat bumetanide-sensitive cotransporter (rBSC1) was examined by Western blotting during the hyponatremia and the subsequent treatment. RESULTS: We noted a markedly high expression of rBSC1 during the development of hyponatremia, and a relatively low expression during vasopressin escape. OPC-31260 administration elevated serum sodium level in a dose-dependent manner. The therapeutic effect, however, declined with increasing number of treatment days, and doses higher than 15 mg/kg/day induced severe toxicity. The physiologic parameters and the alterations of AQP2 and rBSC1 expression during the treatment demonstrated reactions that were completely opposite to those of vasopressin escape. Combination of a furosemide (100 mg/kg/day) and a low dose of OPC-31260 (5 mg/kg/day) additively elevated serum sodium level and sustained the elevated serum sodium level by significantly reducing sodium accumulation in the renal medulla. CONCLUSION: AVP-induced alterations of rBSC1 expression, as well as those of AQP2, are involved in the pathogenesis of SIADH. The pharmacologic blockade of AVP stimulus in SIADH limits its therapeutic efficacy by discontinuing the vasopressin escape, and the selective inhibition of rBSC1 complements this limitation.

Animals↗
PubMed1984

Arteriovenous difference of plasma vasopressin in normal man and effect of posture.

In 13 normotensive 50-year-old men arterial plasma vasopressin (11.3 +/- 2.1 ng/l, mean +/- SE) was significantly increased over venous (7.8 +/- 1.4 ng/l) in the supine position with an arteriovenous difference of 3.5 +/- 1.2 ng/l (p less than 0.05). After 30 min in the upright position, an average increment of 45% to 11.3 +/- 1.8 ng/l was observed for venous vasopressin. Since a similar increase was not found for arterial vasopressin, the arteriovenous difference decreased with 29% to 2.5 +/- 2.1 ng/l and was no longer statistically significant. The correlation between supine and standing vasopressin was statistically significant both for arterial (p less than 0.001) and venous plasma (p less than 0.05). These data indicate a substantial removal of plasma vasopressin by receptors even in the peripheral vascular beds (forearm) and not only in the liver and the kidneys as previous literature claims. The arteriovenous difference decreases in the upright position, most likely because of reduced plasma vasopressin clearance.

Arginine Vasopressin↗
PubMed1993

Renal and central vasopressin receptors: immunocytochemical localization.

Employing an anti-vasopressin monoclonal antibody for immunization, anti-idiotypic monoclonal antibodies were obtained which induced plasminogen activator production in the renal epithelial cell line LLC-PK1. The anti-idiotypic antibodies were employed to visualize vasopressin receptors on LLC-PK1 and A7r5 smooth muscle cells by immunofluorescence. All results indicated specificity of the anti-idiotypes for both V1 and V2 vasopressin receptor subtypes. These antibodies were used for immunohistochemical localization of vasopressin receptors in rat and bovine kidney preparations. In accordance with earlier physiological and biochemical observations, vasopressin receptors were detected predominantly in collecting ducts in cortex and medulla. On the cellular level, a differential staining pattern was observed. On rat brain tissue sections, dense staining was observed within various circumventricular organs. The staining pattern corresponded to that obtained in autoradiographic studies with labeled AVP(4-9) fragment peptide and differed from the distribution of binding sites for labeled vasopressin or V1 antagonists.

Animals↗
PubMed1976

Changes in urinary water and electrolyte excretion in sodium-loaded sheep in response to intravenous infusion of arginine vasopressin.

Mature sheep receiving supplements of sodium chloride into the rumen were given intravenous infusions of arginine vasopressin at rates varying from 4-6-23 pmol/min (2-10 mU/min). Infusion of the hormone led to an increase in urine flow and to increases in the amounts of sodium and chloride excreted, the effect on flow was, however, the greater so that the osmolality of the urine fell during the infusions. In sheep given intravenous infusions of a hypertonic sodium chloride solution addition of vasopressin to the infusate led to the formation of a larger volume of urine containing a higher proportion of the infused salt load compared to when the salt solution alone was given. As before the effect on flow was the greater and hence the osmolality of the urine was lower when the hormone was given. In other experiments intravenous infusion of a hypertonic sodium chloride solution at rates providing 2-8 mmol NaCl/min led to increases in urine flow and increases in sodium and chloride excretion, the size of these increases being proportional to infusion rate. Plasma vasopressin levels markedly increased during these infusions, the levels seen being similar to those seen in sheep given vasopressin in amounts which increased both urine flow and electrolyte excretion. This suggests that during hypertonic salt loading vasopressin probably contributes directly to the increases in urine flow and the increases in electrolyte excretion which are seen. Further evidence in support of this was obtained in experiments in which a greater natriuretic response was seen in sheep given a hypertonic sodium chloride solution into the carotid artery as opposed to the given a hypertonic sodium chloride solution into the carotid artery as opposed to the jugular vein and where it was shown that plasma vasopressin levels were indeed higher when the solution was given into the artery.

Angiotensin II↗
PubMed1987

Evidence supporting a role for endogenous vasopressin in fever suppression in the rat.

1. Infusion of human purified interleukin-1 into a lateral cerebral ventricle of the rat evoked a rise in core temperature which was abolished by heating the interleukin-1. 2. When the intracerebroventricular infusion of interleukin-1 was preceded by a bilateral injection of saline into the ventral septal area, the resulting febrile response was not different from that induced by interleukin-1 alone. However, when the vasopressin V1 antagonist, d(CH2)5Tyr(Me)AVP, was injected into the ventral septal area prior to interleukin-1, a fever was evoked which was significantly greater in magnitude and duration. This enhancement of fever by the V1 antagonist was dose related. 3. Injection of either saline or the V1 antagonist into the ventral septal area, in the absence of interleukin-1, did not evoke any consistent alteration in the core temperature of the rats. 4. The vasopressin V2 antagonist, d(CH2)5-D-ValVAVP, was injected into the ventral septal area to determine the effect of another vasopressin analogue on the fever evoked by interleukin-1. The V2 antagonist did not alter the time course of interleukin-1-induced fever or alter core temperature in the afebrile rat. 5. These data are consistent with the hypothesis that endogenous vasopressin, released in the ventral septal area, may be involved in limiting fever. In addition, these results indicate that the central receptor mediating the antipyretic action of vasopressin may resemble the V1 subtype of peripheral vasopressin receptor.

Animals↗
PubMed1985

Vasopressin-stimulated release of atriopeptin: endocrine antagonists in fluid homeostasis.

Administration of pharmacological doses of arginine-vasopressin, related peptides, and other pressor agents induced a profound release of atriopeptin immunoreactivity into the circulation. The stimulated release of atriopeptin apparently was related to increased arterial blood pressure. Neither the nonpressor vasopressin analog 1-deamino-D-Arg8-vasopressin nor arginine-vasopressin in the presence of a specific pressor antagonist caused atriopeptin to be released into the circulation. Urine output was correlated with the level of atriopeptin released. Physiological levels of arginine-vasopressin suppress diuresis and produced vasoconstriction. Pharmacological levels of the hormone stimulated the cardiac endocrine system to release atriopeptin, which may cause diuresis and vasodilation to physiologically antagonize the effects of vasopressin.

Adrenocorticotropic Hormone↗
PubMed1993

Bombesin treatment enhances vasopressin receptors in Swiss 3T3 cells.

Cells possess receptors for multiple different peptides that regulate a wide spectrum of biological processes. Although examples of homologous and heterologous downregulation have been reported, relatively little is known about the interaction between different peptides in modulating cellular activities. Here we demonstrate that pretreatment of Swiss 3T3 fibroblasts with 10 nM bombesin for 48 h enhanced the 45Ca2+ efflux acutely stimulated by vasopressin. The effect was not reciprocal, since preincubation with vasopressin did not affect the bombesin-stimulated Ca2+ efflux. Measurement of displaceable [3H] vasopressin binding demonstrated that bombesin pretreatment increases the hormonal binding by 3.8 +/- 0.2-fold (SE; n = 14) measured at 37 degrees C or at 4 degrees C. Scatchard analysis at 4 degrees C indicated that the increased binding reflects an increase in the number of vasopressin receptors without any significant effect on the apparent affinity of binding. Furthermore, addition of cycloheximide completely prevented the increase in [3H] vasopressin binding induced by bombesin. We conclude that long-term bombesin pretreatment induces heterologous enhancement of vasopressin responsiveness by increasing the number of membrane receptors.

3T3 Cells↗
PubMed2004

Attenuation of vasopressin-induced antidiuresis in poorly controlled type 2 diabetes.

Renal resistance to vasopressin has been demonstrated in type 1 diabetes and in type 2 diabetes with nephropathy. However, renal response to vasopressin in type 2 diabetes without nephropathy has not been studied. We studied 10 subjects with poorly controlled type 2 diabetes (PCDS; Hb A(1c) >9%), 10 subjects with well-controlled type 2 diabetes (WCDS; Hb A(1c) <7%), and 10 matched nondiabetic control subjects (NDCS) during a euglycemic 8-h water deprivation test. None of the subjects had nephropathy. Water deprivation caused similar rises in plasma vasopressin concentrations in all three groups, but the rise in urine osmolality in PCDS (280.3 +/- 49.7 to 594.4 +/- 88.5 mosmol/kgH(2)O) was lower than in WCDS (360.7 +/- 142.8 to 794.1 +/- 77.3 mosmol/kgH(2)O, P < 0.001) or NDCS (336.0 +/- 123.3 to 786.5 +/- 63.3 mosmol/kgH(2)O, P = 0.019). Total urine output was higher in the PCDS than in WCDS and NDCS (P < 0.05). Linear regression analysis showed that, in PCDS, the osmotic thresholds for thirst (291.9 +/- 4.6 mosmol/kgH(2)O) and vasopressin release (291.1 +/- 2.9 mosmol/kgH(2)O) were higher compared with WCDS (286.6 +/- 1.8 and 286.0 +/- 3.6 mosmol/kgH(2)O, respectively) and NDCS (286.0 +/- 2.4 and 284.1 +/- 4.7 mosmol/kgH(2)O, respectively) (between groups P < 0.001 for both variables). Under conditions of euglycemia, PCDS have impaired renal response to vasopressin and elevated osmotic threshold for thirst and vasopressin release in response to dehydration. Under conditions of chronic hyperglycemia, these abnormalities may significantly contribute to the development of dehydration in PCDS.

Aged↗
PubMed1992

Upregulation of V1a vasopressin receptors by glucocorticoids.

WRK1 cells (a rat mammary tumor cell line) exhibit a vasopressinergic receptor of V1a subtype tightly coupled to phospholipase C. Addition of dexamethasone to the culture medium principally potentiated the vasopressin-sensitive accumulation of inositol phosphates and to a lesser extent the NaF-sensitive phospholipase C activity. On the opposite, such treatment was without effect on the basal level of intracellular inositol phosphates or on bradykinin- or serotonin-sensitive phosphoinositide metabolisms. Glucocorticoid receptors were probably involved in these actions since dexamethasone was found to be more potent than aldosterone or corticosterone. Dexamethasone treatment also increased the number of vasopressin binding sites without affecting its affinity for vasopressin or other specific vasopressin analogues. These results strongly suggest that dexamethasone principally acts at the vasopressin receptor level by affecting its synthesis and/or the translation of its mRNA and also affects the G protein that couples the V1a receptor to the phospholipase C. These results explain how glucocorticoids may regulate the transduction mechanisms involved in vasopressin actions on WRK1 cells. They provide explanations for understanding the cross talk between adrenal steroids and hormones, which mobilize intracellular calcium.

Animals↗
PubMed1992

CNS vasopressin mediates emotional stress and CRH-induced colonic motor alterations in rats.

The effects of emotional stress (ES) corresponding to conditioned fear on colonic motility and its antagonism by [deamino-Pen1, Val4, D-Arg8]vasopressin, a vasopressin antagonist, were investigated by electromyography in conscious fasted rats fitted with chronically implanted electrodes. A 117% increase (19.6 +/- 2.1 vs. 9.0 +/- 0.9 cycles/10 min during the control period) in the frequency of colonic spike bursts was observed when rats were placed for 30 min in a box in which they had previously received electric foot shocks. Intracerebroventricular (icv) administration of corticotropin-releasing hormone (CRH; 0.5 micrograms/kg) mimicked the effects of ES and increased the spike burst frequency of the colon by 88.6% from 5 to 15 min after its administration. At doses between 5 and 20 micrograms/kg the antagonist [deamino-Pen1, Val4, D-Arg8]vasopressin significantly reduced or abolished the effects of ES and CRH administration on colonic motility. Injected icv at doses of 2.5 and 5 ng/kg [Arg8]vasopressin dose dependently increased the frequency of colonic spike bursts. These effects were not reproduced by similar or higher (50 ng/kg) doses given intraperitoneally, and the effects were abolished after previous administration of vasopressin at a dose of 20 micrograms/kg. It is concluded that the effects of ES on colonic motility in rats previously shown to be linked to the central nervous system (CNS) release of CRH are in turn mediated through the central release of vasopressin.

Animals↗
PubMed1999

Role of the vasopressin V(1) receptor in regulating the epithelial functions of the guinea pig distal colon.

Vasopressin has a wide spectrum of biological action. In this study, the role of vasopressin in regulating electrolyte transport in the colon was elucidated by measuring the short-circuit current (I(sc)) as well as the Na(+), K(+), and Cl(-) flux in a chamber-mounted mucosal sheet. The cytosolic Ca(2+) concentration ([Ca(2+)](i)) was also measured in fura 2-loaded cells by fluorescence imaging. Serosal vasopressin decreased I(sc) at 10(-9) M and increased I(sc) at 10(-7)-10(-6) M. The decrease in I(sc) was accompanied by two effects: one was a decrease in the amiloride-sensitive Na(+) absorption, whereas the other was an increase in the bumetanide-sensitive K(+) secretion. The increase in I(sc) was accompanied by an increase in the Cl(-) secretion that can be inhibited by serosal bumetanide or mucosal diphenylamine-2-carboxylate. Vasopressin caused an increase in [Ca(2+)](i) in crypt cells. These responses of I(sc) and the [Ca(2+)](i) increase in crypt cells were all more potently inhibited by the vasopressin V(1) receptor antagonist than by the V(2) receptor antagonist. These results suggest that vasopressin inhibits electrogenic Na(+) absorption and stimulates electrogenic K(+) and Cl(-) secretion. In all of these responses, the V(1) receptor is involved, and the [Ca(2+)](i) increase may play an important role.

Absorption↗
PubMed1982

Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats.

We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. In fact, heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Moreover, fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the base line and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.

Animals↗
PubMed1985

Reflexes fail to reduce pressor activity of vasopressin in spontaneous hypertension.

Pressor responses and heart rate responses were recorded in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto (WKY) rats during intravenous infusions of arginine vasopressin and phenylephrine under two experimental situations, first when cardiovascular reflexes were impaired by pretreatment with a ganglionic blocking agent (pentolinium) and second, when reflexes remained intact. In rats with ganglia blocked, pressor responses of SHR to vasopressin or to phenylephrine were similar to those of WKY rats. In rats with intact reflexes, pressor responses of SHR to phenylephrine were also similar to those of WKY rats but, in contrast, pressor responses of SHR to vasopressin were enhanced. Heart rate fell much more for any given elevation of blood pressure in WKY rats than in SHR during infusions of vasopressin and phenylephrine, and the bradycardia associated with these pressor agents was largely abolished by pentolinium. The results are consistent with the hypothesis that baroreflexes buffer the pressor activity of vasopressin in the normotensive WKY rat and that an impairment of baroreflex activity in SHR contributes to the enhanced pressor activity of vasopressin in these rats.

Animals↗
PubMed1987

Vasoconstrictor role for vasopressin in conscious, sodium-depleted rats.

To define the role of vasopressin as a vasoconstrictor hormone in sodium depletion, systemic hemodynamics and regional blood flow distribution were examined in conscious Sprague-Dawley rats after 6 days of a low-sodium diet. Studies were performed after selective or combined blockade with the vasopressin antagonist [d(CH2)5Tyr(Me)]AVP (AVPA), enalaprilat (CEI), and phentolamine (PHENTOL). Plasma levels of vasopressin were increased significantly after CEI and increased further after PHENTOL and CEI plus PHENTOL. AVPA had no effect on blood pressure, whether given alone or in the presence of PHENTOL, CEI, or CEI plus PHENTOL. Significant falls in peripheral vascular resistance associated with reflex increases in cardiac output were observed when AVPA was given to animals pretreated with either CEI or PHENTOL but not both. AVPA alone produced no significant changes in regional blood flow distribution, but a vasoconstrictor action of vasopressin in the renal vascular bed was revealed after prior treatment with CEI or PHENTOL. Muscle blood flow was also increased in the PHENTOL plus AVPA group compared with the PHENTOL group. No significant additional effects of AVPA were revealed by pretreatment with CEI, PHENTOL, or CEI plus PHENTOL for mesenteric, hepatic, splenic, or cerebral vascular beds. It is suggested that vasopressin acts as a vasoconstrictor hormone in conscious sodium-depleted rats when either the renin-angiotensin system or alpha-adrenergic system is inhibited but not when both systems are blocked. The renal vascular bed is an important site for vasopressin-induced vasoconstriction under these circumstances.

Adaptation, Physiological↗
PubMed1989

Pressor responses to vasopressin in pigs and sheep with DOCA hypertension.

Pressor responses to vasopressin were determined in pigs and sheep during three experimental periods: 1) before deoxycorticosterone acetate (DOCA) treatment, 2) 21 days after DOCA implantation (100 mg/kg) when a stable hypertension had developed, and 3) after reversal of the hypertension by removing the implant in the sheep or by decreasing the dietary sodium intake in the pigs. The infusion of lysine (LVP) or arginine (AVP) vasopressin into pigs and sheep, respectively, resulted in dose-dependent increases in plasma vasopressin concentration. The levels of plasma LVP or AVP achieved by these infusions were not altered in any of the experimental periods. The administration of vasopressin resulted in dose-dependent increases in mean arterial blood pressure. However, pigs required five times more LVP than sheep required AVP to achieve similar pressor responses. The pressor responsiveness to vasopressin was attenuated when either species was made hypertensive. This effect was reversed when normal blood pressure was restored by reducing sodium intake in the pigs or by removing the DOCA implant from the sheep. These data establish that an increased pressor response to vasopressin does not contribute to DOCA hypertension in pigs or sheep.

Animals↗
PubMed1992

Endothelial L-arginine pathway and regional cerebral arterial reactivity to vasopressin.

Experiments were designed to characterize the mechanism of vasopressin action in small arteries of brain stem and cerebrum and to determine the role of L-arginine pathway in reactivity of these vessels to vasopressin. Secondary branches of canine basilar arteries (425 +/- 63 microns ID, n = 6) and middle cerebral arteries (466 +/- 30 microns ID, n = 6) were dissected and mounted on glass microcannulas in organ chambers. Changes in intraluminal diameter of the pressurized arteries were measured using a video dimension analyzer. Vasopressin caused endothelium-dependent relaxation in the brain stem arteries [-log half-maximal effective concentration (EC50) = 9.2 +/- 0.4, n = 5] but not in the branches of middle cerebral arteries. In contrast, bradykinin caused identical endothelium-dependent relaxations in arteries of both regions (-log EC50 = 8.0 +/- 0.2, n = 5, and 7.7 +/- 0.1, n = 4 for brain stem and cerebrum, respectively). Relaxations to vasopressin (but not to bradykinin) were reduced in the presence of V1-vasopressinergic antagonist [1-(beta-mercapto-beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5-Tyr(Me)AVP;10(-7) M], pertussin toxin (100 ng/ml), and NG-monomethyl-L-arginine (L-NMMA; 10(-4) M). The inhibitory effect of L-NMMA was prevented by L-arginine (3 x 10(-4) M) but not D-arginine (3 x 10(-4) M). These studies suggest that vasopressin causes endothelium-dependent relaxation in canine brain stem arteries. The effect of the neuropeptide appears to be mediated by activation of endothelial V1-vasopressinergic receptors coupled to nitric oxide synthase. This signal transduction pathway is not functional in endothelial cells of branches of middle cerebral arteries.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

Involvement of prostaglandin E2, cAMP, and vasopressin in lithium-induced polyuria.

The involvement of prostaglandin E2 (PGE2), adenosine 3',5'-cyclic monophosphate (cAMP), and vasopressin in lithium-induced polyuria was investigated in rats. Administration of LiCl (4 mmol/kg body wt) for 7 days induced a marked polyuria with a significant excretion of urinary PGE2. Administration of indomethacin (IND, 5 mg/kg body wt) for 4 days to lithium-induced diabetes insipidus (LiDI) rats diminished urine volume by 80% and urinary PGE2 by 85%. The in vitro data of the intact rat kidney showed that lithium stimulated arginine vasopressin (AVP)-induced PGE2 production and suggested that PGE2 suppressed cAMP synthesis in rat renal medulla. The AVP-induced PGE2 synthesis was greater and the AVP-stimulated cAMP production lower in the LiDI rat kidney in vitro. Interference of the vasopressin-associated cAMP system and the increased PGE2 synthesis in the kidney may be involved in the development of LiDI. The reduced cAMP production in the LiDI rat kidney might be partly due to the increased PGE2 synthesis. In LiDI rats plasma vasopressin increased, whereas AVP concentration in the hypothalamus and the neurohypophysis significantly decreased. It is postulated that lithium stimulates vasopressin release from the central nervous system and that elevated plasma vasopressin potentiates PGE2 production in the kidney synergistically with lithium.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Control of renal medullary blood flow by vasopressin V1 and V2 receptors.

Experiments were performed in anesthetized renal-denervated rats to determine the contribution of renal medullary vasopressin V1 and V2 receptor stimulation in the regulation of renal medullary blood flow. Renal medullary interstitial infusion of the selective V1 agonist [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1) significantly decreased outer medullary blood flow by 15% and inner medullary blood flow by 35%, as measured with implanted optical fibers for laser-Doppler flowmetry. Medullary interstitial infusion of equimolar doses of arginine vasopressin (AVP) also decreased outer medullary blood flow by 15% but decreased inner medullary blood flow by only 17%, a decrease significantly less than that during the infusion of the V1 agonist. These results were confirmed in videomicroscopy experiments on the exposed papilla, which demonstrated that the V1 agonist and AVP decreased descending and ascending vasa recta capillary red blood cell velocity and calculated blood flow, with greater decreases during infusion of the V1 agonist. In further laser-Doppler flowmetry studies, stimulation of V2 receptors by medullary interstitial infusion of 1-desamino-8-D-arginine vasopressin (2 ng.kg-1.min-1) or AVP in rats pretreated with the vasopressin V1 receptor antagonist d(CH2)5[Tyr(Me)2,Ala-NH2]AVP increased renal medullary blood flow by 16 +/- 3 and 27 +/- 8%, respectively. The present experiments indicate that vasopressin V1 receptor stimulation serves to decrease renal medullary blood flow while V2 receptor stimulation appears to increase renal medullary blood flow; however, the net effect of AVP is to decrease renal medullary blood flow.

Animals↗