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PubMed1997

Mechanism of vasopressin-induced increase in intracellular Ca2+ in LLC-PK1 porcine kidney cells.

Analysis of the signal transduction cascade of vasopressin-induced increase in intracellular Ca2+ concentration ([Ca2+]i) in LLC-PK1 cells was performed. First, a comparison of the effect of vasopressin on [Ca2+]i in LLC-PK1 cells with that produced in rat hepatocytes was performed [an intracellular mobilizing mechanism involving a V1 receptor coupled to the production of inositol 1,4,5-trisphosphate (IP3)]. Second, the effect of known inhibitors of intracellular Ca2+ mobilization on vasopressin Ca2+ response in LLC-PK1 cells was studied. Vasopressin induced a transient increase in [Ca2+]i in both LLC-PK1 cells and hepatocytes. In contrast to the single [Ca2+]i spike seen in LLC-PK1 cells, vasopressin induced an average of two to three [Ca2+]i spikes in hepatocytes. The V1 antagonist (Pmp1-O-Me-Tyr2-[Arg8]vasopressin, 1 microM) abolished vasopressin Ca2+ response in both cell types. Inhibitors of intracellular Ca2+ mobilization, thapsigargin (5 microM) and U-73122 (3 microM), abolished the Ca2+ response by vasopressin in LLC-PK1 cells. The results suggest that vasopressin-induced increase in [Ca2+]i in LLC-PK1 cells is mediated via a V1-like receptor and involves the mobilization of intracellular Ca2+ through an IP3- or thapsigargin-sensitive Ca2+ pool.

Animals↗
PubMed1983

Vasopressin and angiotensin II receptors in rat aortic smooth muscle cells in culture.

Rat aortic smooth muscle cells were isolated and maintained in primary culture. After 2-3 days, cells recovered their contractile phenotype and could be induced to contract in response to vasopressin and angiotensin II. Vasopressin- and angiotensin-specific binding sites were detected on these cells, using tritiated Lys8-vasopressin, Asn1-Val5-angiotensin II, and Sarc1-Ile8-angiotensin II. Vasopressin binding sites had Kd values of 30 and 12 nM for Lys8-and Arg8-vasopressin, respectively, and a maximal binding capacity of 25,000 sites/cell. They displayed several of the expected characteristics of vasopressin receptors involved in the vasopressor response in vivo. A highly significant correlation was found between the relative agonistic or antagonistic vasopressor potencies of a series of vasopressin structural analogues and their relative abilities to inhibit [3H]vasopressin binding to aortic smooth muscle cells. Specific binding sites for Asn1-Val5-angiotensin II and Sarc1-Ile8-angiotensin II had the following characteristics: Kd = 2.3 and 1.3 nM, respectively; maximal capacity: 50,000 sites/cell. Vasopressin and angiotensin did not modify the intracellular cyclic AMP content of aortic smooth muscle cells.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1994

Effect of endogenous vasopressin on blood flow to choroid plexus during hypoxia and intracranial hypertension.

Exogenous vasopressin decreases blood flow to the choroid plexus and production of cerebrospinal fluid. Some studies indicate that hypoxia and increases in intracranial pressure (ICP) produce increases in circulating vasopressin. We examined the hypothesis that endogenous release of vasopressin decreases blood flow to the choroid plexus during hypoxia and increased ICP. Blood flow to the choroid plexus was measured in anesthetized rabbits using microspheres. Hypoxia increased cerebral blood flow more than twofold but had little effect on blood flow to the choroid plexus. In contrast, hypoxia produced a marked increase in blood flow to the choroid plexus in the presence of a vasopressin V1-antagonist, [d(CH2)5Tyr(Me)]AVP. During intracranial hypertension, blood flow to the choroid plexus decreased from 409 +/- 42 to 295 +/- 25 ml.min-1 x 100 g-1 (means +/- SE; P < 0.05 vs. control) when ICP was increased from 1 to 40 mmHg. The vasopressin antagonist inhibited the decrease in blood flow to the choroid plexus in response to increased ICP. Thus release of vasopressin during hypoxia and increased ICP have a constrictor effect on blood vessels of the choroid plexus. Plasma levels of vasopressin increased minimally during hypoxia and increased ICP, which suggests that sources of vasopressin other than plasma affect blood vessels of the choroid plexus. We propose that endogenous vasopressin may play a protective role during hypoxia and intracranial hypertension by a negative feedback mechanism to reduce blood flow to the choroid plexus.

Animals↗
PubMed1993

Vasopressin and oxytocin receptors coupled to Ca2+ mobilization in rat inner medullary collecting duct.

In renal collecting duct epithelial cells, arginine vasopressin (AVP) at greater than nanomolar concentrations has been reported to transiently increase intracellular free calcium ([Ca2+]i) in a manner consistent with activation of the phosphoinositide pathway. To investigate whether any of the known neurohypophysial hormone subtypes are involved, we measured [Ca2+]i in microdissected rat terminal inner medullary collecting duct (IMCD) using fura-2. To allow quantitative comparisons of the response under different conditions, we determined the areas under the response curves (in nM.min) over 1.5 min using numerical integration. AVP, the V1b-receptor agonist [deamino1,D-3-(pyridyl)Ala2,Arg8]vasopressin, the V2-receptor agonist 1-desamino-8-D-arginine vasopressin, oxytocin, and the selective oxytocin-receptor agonist [Thr4,Gly7]oxytocin (TG-OXT), each at 10 nM, significantly increased [Ca2+]i (69.52 +/- 10.25, 27.0 +/- 11.7, 24.33 +/- 5.83, 14.75 +/- 2.81, and 14.57 +/- 3.50 nM.min, respectively). In contrast, a V1a-selective agonist ([Phe2,Ile3,Orn8]vasopressin) did not increase [Ca2+]i (0.43 +/- 2.36 nM.min). In desensitization studies, challenge with 10 nM AVP or TG-OXT completely prevented a rise in [Ca2+]i in response to immediate rechallenge with the same agent, but not the other, demonstrating homologous desensitization. The lack of cross-desensitization implies that at least two receptors are present that can trigger a rise in [Ca2+]i in response to neurohypophysial hormones. Antagonists for oxytocin ([des-glycinamide9,d(CH2)5(1),O-Me-Tyr2,Thr4,Orn8]vaso tocin), V2 ([d(CH2)5(1),D-Ile2,Ile4,Arg8]vasopressin), and V1a ([d(CH2)5(1),O-Me-Tyr2,Arg8]vasopressin) receptors partially inhibited the [Ca2+]i response induced by 10 nM AVP (89.5, 81.6, and 51.4% inhibition, respectively). These data are consistent with the view that both an oxytocin receptor and a vasopressin receptor are coupled to a [Ca2+]i mobilization response in rat terminal IMCD. This vasopressin receptor is distinct from both the V1a receptor and the V2 receptor and may be either the V1b receptor or a novel vasopressin receptor subtype.

Animals↗
PubMed1988

Contribution of vasopressin in dexamethasone-induced hypertension in rats.

Our previous finding that dexamethasone-induced hypertension in rats is associated with enhanced reactivity of mesenteric arteries to arginine vasopressin but not to angiotensin II (Ang II) or norepinephrine has led us to postulate that vasopressin contributes to the development or maintenance of glucocorticoid-induced hypertension. To test this view, we investigated the effects of vasopressin, Ang II, norepinephrine, and the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP on mean arterial blood pressure and heart rate with and without ganglionic blockade with hexamethonium and angiotensin I (Ang I) converting enzyme inhibition with MK 421 in pentobarbital-anesthetized rats made hypertensive by treatment with dexamethasone (1.8 mg/kg/wk for 14 days). Administration of vasopressin, Ang II, or norepinephrine (0.003-3 microgram i.v.) produced a dose-related increase in arterial blood pressure. The pressor response to vasopressin, but not to Ang II or norepinephrine, was greater in dexamethasone-treated than in vehicle-treated animals, and this difference became more pronounced in rats that received hexamethonium and MK 421. Administration of the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP significantly reduced arterial pressure in dexamethasone-treated but not in vehicle-treated animals. Hexamethonium and MK 421 reduced arterial blood pressure in dexamethasone-treated as well as in vehicle-treated rats; however, arterial blood pressure remained higher in the former. Administration of the vasopressin V1 receptor antagonist produced a greater reduction in arterial blood pressure in dexamethasone-treated than in vehicle-treated rats. These data suggest that vasopressin contributes to glucocorticoid-induced hypertension, which is probably due to enhanced vascular reactivity to the peptide.

Angiotensin II↗
PubMedDate not supplied

Norepinephrine-induced potentiation of arginine vasopressin reactivity in arterioles of the spontaneously hypertensive rat.

We have studied microvascular reactivity to vasopressin alone and in combination with norepinephrine in young (6- to 8-week-old) spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) controls. Closed-circuit TV microscopy was used to quantify the in vivo diameter responses of small arterioles (17 to 26 mu) to vasopressin (1.25 X 10(-8) to 3.75 X 10(-7) M) injected intraarterially alone and with simultaneous topical suffusion of a subthreshold concentration of norepinephrine in the cremaster muscle microcirculation. Percent decrease in luminal diameter was integrated over a 30-second period to obtain log concentration response curves. The vasoconstrictor response to vasopressin was concentration-dependent in both groups (p less than 0.001). A significant increase in reactivity to vasopressin alone was exhibited by the SHR arterioles compared to the WKY vessels (p less than 0.02). Maximum constriction was 55% higher in the SHR (p less than 0.04). The SHR also demonstrated a greater sensitivity to vasopressin (p less than 0.02). Vasopressin-induced vasoconstriction was potentiated by norepinephrine in the SHR, demonstrated by the significant shift of the curve up and to the left of the SHR response curve to vasopressin alone (p less than 0.01). The maximum response was 38% greater (p less than 0.02). Sensitivity was significantly enhanced (p less than 0.01). Additionally, the presence of norepinephrine stimulated a three-fold greater incidence of complete closure. In contrast to SHR results, topical suffusion of norepinephrine did not significantly alter the reactivity of the WKY arterioles to vasopressin-induced constriction. Our results support a role for vasopressin as a potential vasoconstrictor in the developing stage of SHR hypertension which may be modulated by norepinephrine and thus contribute to the elevated total peripheral resistance observed.

Administration, Topical↗
PubMed1984

The role of vasopressin and the sympathetic nervous system in the cardiovascular response to vagal cold block in the conscious dog.

This study examined the role of arginine vasopressin in the pressor response to vagal cold block and evaluated a possible interaction between vasopressin and the sympathetic nervous system during vagal block in conscious dogs with (carotid sinus intact) and without (sinoaortic denervated) functional arterial baroreflexes. In both carotid sinus intact and sinoaortic denervated dogs, elimination of the arginine vasopressin pressor system by the specific vasopressin antagonist d(CH2)5Tyr(Me)AVP did not alter the response to vagal block, as evaluated by changes in arterial pressure. Subsequent removal of the sympathetic nervous system by ganglionic blockade abolished the response to vagal block. When ganglionic blockade was induced in the absence of the vasopressin antagonist, the pressor response to vagal block was reduced by only 60%. Arginine vasopressin antagonist after ganglionic blockade reduced the response to vagal block by an amount equivalent to 45% of the original increase in pressure. The effects of blockade of either vasopressin or the sympathetic nervous system on the pressor response to vagal block were significantly greater when the other system had previously been eliminated. Data suggest that both arginine vasopressin and the sympathetic nervous system contribute to the pressor response to vagal block. One interpretation of these results is that vasopressin also interacts centrally to inhibit sympathetic outflow and thus modulates the hemodynamic manifestation of interruption of vagal afferents.

Animals↗
PubMed1984

In vitro adrenocorticotropin/beta-endorphin-releasing activity of vasopressin analogs is related neither to pressor nor to antidiuretic activity.

The ability of vasopressin and related analogs to induce ACTH, beta-endorphin, and beta-lipotropin release was studied in vitro using incubated rat anterior pituitary quarters or a perifused rat isolated anterior pituitary cell column. Vasopressin and its analogs exhibited corticotropin-releasing factor (CRF)-like activity in a rank order which was different from those for vasopressor or antidiuretic activity. Two dissimilar antagonists with antivasopressor activity showed different effects: one possessed CRF-like activity itself, the other blocked the CRF-like activity of vasopressin. Another antagonist with antipressor and also antiantidiuretic activity had no effect when given alone and also didn't block the CRF-like activity of vasopressin. Some analogs were also tested for their effects on cAMP accumulation. Analogs, which possessed CRF-like activity or blocked CRF-like activity of vasopressin, stimulated cAMP accumulation or inhibited vasopressin-stimulated cAMP accumulation in anterior pituitary quarters, respectively. These results imply that the structural requirements of the CRF-like activity of vasopressin differ from those of the pressor and antidiuretic activity. Therefore, it is possible that the pituitary receptors responsible for CRF-like activity of vasopressin represent a separate category of vasopressin receptors which may be linked to an adenylate cyclase.

Adrenocorticotropic Hormone↗
PubMed1986

The metabolic clearance rate of and pressor responses to vasopressin in male and female rats.

Recent evidence indicates that the plasma vasopressin concentration is higher in males than in females and that this may be due to sexually dimorphic effects of the gonadal steroids. However, whether this difference in plasma vasopressin levels reflects differences in secretion or metabolism of the hormone could not be determined from the available data. Therefore, we measured the MCR of vasopressin in conscious male and female rats over a broad range of plasma concentrations of the hormone. No differences were observed in MCR either within a sex or between the sexes over the ranges of plasma concentrations of vasopressin tested. This indicates that the differences in basal plasma vasopressin concentration that were previously reported between male and female rats reflect differences in secretion. In addition, the pressor responses to infused vasopressin were 2 to 3 times greater (P less than 0.01) in male than in female rats, even though the plasma vasopressin concentrations achieved in the two groups were identical. Although the basal heart rate was higher (P less than 0.01) in female than in male rats, the decreases in heart rate observed in response to the vasopressin infusions were similar between the sexes. The mechanisms responsible for the differences in basal vasopressin secretion and pressor responsiveness between males and females are uncertain, but could involve actions of the gonadal steroids on the central nervous system and the peripheral vasculature.

Animals↗
PubMed1998

Variable expression of the V1 vasopressin receptor modulates the phenotypic response of steroid-secreting adrenocortical tumors.

We studied the putative role of the vasopressin receptors in the phenotypic response of steroid-secreting adrenocortical tumors. A retrospective analysis of a series of 26 adrenocortical tumors responsible for Cushing's syndrome (19 adenomas and 7 carcinomas) showed that vasopressin (10 IU, i.m., lysine vasopressin) induced an ACTH-independent cortisol response (arbitrarily defined as a cortisol rise above baseline of 30 ng/mL or more) in 7 cases (27%). In comparison, 68 of 90 patients with Cushing's disease (76%) had a positive cortisol response. We then prospectively examined the expression of vasopressin receptor genes in adrenocortical tumors of recently operated patients (20 adenomas and 19 adrenocortical carcinomas). We used highly sensitive and specific quantitative RT-PCR techniques for each of the newly characterized human vasopressin receptors: V1, V2, and V3. The V1 messenger ribonucleic acid (mRNA) was detected in normal adrenal cortex and in all tumors. Its level varied widely between 2.0 x 10(2) and 4.4 x 10(5) copies/0.1 microgram total RNA, and adenomas had significantly higher levels than carcinomas, although there was a large overlap. Among the 6 recently operated patients who had been subjected to the vasopressin test in vivo, the tumor V1 mRNA levels were higher in the 4 responders (9.5 x 10(3) to 5.0 x 10(4)) than in the 2 nonresponders (2.0 x 10(2) and 1.8 x 10(3)). One adenoma that had a brisk cortisol response in vivo, also had in vitro cortisol responses that were inhibited by a specific V1 antagonist. In situ hybridization showed the presence of V1 mRNA in the normal human adrenal cortex where the signal predominated in the compact cells of the zona reticularis. A positive signal was also present in the tumors with high RT-PCR V1 mRNA levels; its distribution pattern was heterogeneous and showed preferential association with compact cells. RT-PCR studies for the other vasopressin receptors showed a much lower signal for V2 and no evidence for V3 mRNA. We could not establish whether the V2 mRNA signal observed in normal and tumoral specimens was present within adrenocortical cells or merely within tissue vessels. We conclude that the vasopressin V1 receptor gene is expressed in normal and tumoral adrenocortical cells. High, and not ectopic, expression occurs in a minority of tumors that become directly responsive to vasopressin stimulation tests.

Adenoma↗
PubMed1982

The influence of vasopressin on oxytocin-induced changes in urine flow in the male rat.

Oxytocin administration in rat infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin deficiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.

Animals↗
PubMed1996

Possible contribution of dopaminergic receptors in the anteroventral third ventricular region to hyperosmolality-induced vasopressin secretion in conscious rats.

We have reported previously that regions encompassing the cerebral ventricle may contain dopamine receptors responsible for facilitatory roles in the osmotic release of vasopressin in conscious rats. In order to explore the location of these receptors, we injected (0.5 mul) the dopamine antagonist haloperidol (13.3 nmol) or dopamine (26.4 nmol) topically into the anteroventral third ventricular region or the paraventricular nucleus of rats, and their effects on the levels of plasma vasopressin and its controlling factors were examined in the presence or absence of an osmotic stimulus. The effects of haloperidol injections into the ventral tegmental area were also tested to study whether information associated with drinking behavior may affect the osmotic vasopressin secretion. Intravenous infusion (0.1 ml kg-1 body wt min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin 15 and 30 min later, and this was accompanied by an augmentation of plasma osmolality, sodium and chloride, and by elevated or unaltered arterial pressure. The vasopressin response was abolished by haloperidol injection into the anteroventral third ventricular region 10 min before the beginning of the hypertonic saline infusion. The injection sites were confirmed histologically to have been in or near the organum vasculosum of the laminae terminalis and a ventral part of the median preoptic nucleus. Similarly, a partial but significant reduction of the vasopressin response was noted after bilateral injections of haloperidol into the ventral tegmental area, whereas bilateral haloperidol injections into the paraventricular nucleus had no appreciable effect. The responses of plasma osmolality, electrolytes and arterial pressure to the osmotic load were not affected significantly by haloperidol injections into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. The iv infusion of isotonic saline (0.15 mol/l) did not change plasma vasopressin and the other variables significantly, and this was also the case when preceded by application of haloperidol into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. Dopamine injection into the anteroventral third ventricular region increased plasma vasopressin 5 min later, without affecting plasma osmolality, electrolytes or arterial pressure. On the basis of these results, we concluded that dopamine receptors responsible for facilitatory roles in osmotically stimulated vasopressin secretion may exist in the anteroventral third ventricular region and ventral tegmental area.

Animals↗
PubMed2003

Effect of arginine vasopressin on the canine epicardial coronary artery: experiments on V1-receptor-mediated production of nitric oxide.

OBJECTIVE: To determine whether arginine vasopressin releases endothelium-derived nitric oxide (EDNO) from the epicardial coronary artery. METHODS: We studied segments of canine left circumflex coronary arteries suspended in organ chambers to measure isometric force. The coronary artery segments were contracted with prostaglandin F2alpha (2 x 10-6M) and exposed to a unique, strong arginine vasopressin concentration (10-6M) or titrated concentrations (10-9 a 10-5 M). RESULTS: The unique dose of arginine vasopressin concentration (10-6M) induced transient, but significant (p<0.05), relaxation in arterial segments with endothelium, and an increase, not significant, in tension in arteries without endothelium. Endothelium-dependent relaxation to arginine vasopressin was inhibited by Ng-monomethyl-L-arginine (L-NMMA, 10-5M) or N G-nitro-L-arginine (L-NOARG) (10-4M), 2 inhibitors of nitric oxide synthesis from L-arginine. Exogenous L-arginine (10-4M), but not D-arginine (10-4M), reversed the inhibitory effect of L-NMMA on vasopressin-mediated vasorelaxation. Endothelium dependent relaxation to vasopressin was also reversibly inhibited by the vasopressin V1-receptor blocker d(CH2)5Try(Me) arginine vasopressin (10-6M) (n=6, P<0.05). CONCLUSION: Vasopressin acts through V1 endothelial receptors to stimulate nitric oxide release from L-arginine.

Animals↗
PubMed1988

Platelet aggregation and vasopressin receptors in patients with diabetes mellitus.

Plasma vasopressin, vasopressin-induced platelet aggregation, and platelet vasopressin receptors were investigated in 10 normal subjects and 14 diabetic patients free of microangiopathy. Basal plasma vasopressin concentration was identical in two groups. Platelet aggregation induced by vasopressin as well as by epinephrine was not significantly altered in the diabetic patients. However, exploration of platelet V1-vasopressin receptors revealed in the diabetic group a dramatic reduction in the number of binding sites without alteration of the receptor affinity for tritiated vasopressin. Thus vasopressin-induced platelet aggregation in uncomplicated diabetes mellitus remains normal despite a decrease in the number of vasopressin receptors presumably due to alterations of the platelet membrane structure.

Adult↗
PubMed1992

[Vasopressin (ADH)].

Vasopressin is thought to play an important role, not only in the metabolism of water and electrolytes, but also in the regulation of renal hemodynamics. This year, great progress has been achieved in molecular biology of vasopressin receptors. First, the cloning of a complementary DNA, encoding the rat liver V1a arginine vasopressin receptor, was reported. The liver cDNA encodes a protein with seven putative transmembrane domains, which binds arginine vasopressin and related compounds with affinities similar to the native rat V1a receptor. The messenger RNA, corresponding to the cDNA, is distributed in rat tissues, known to contain V1a receptors. Second, the cloning of a complementary DNA encoding the rat kidney V2 arginine vasopressin receptor was also successful. The kidney cDNA encodes a protein with a transmembrane topography characteristic of G protein-coupled receptors. The receptor messenger RNA is detected only in the kidney. Last year, an orally active and specific vasopressin V1 receptor antagonist, OPC-21268 was first reported. The i.v. or p.o. administration of OPC-21268 dose-dependently inhibited vasopressin-induced vasoconstriction, while that induced by angiotensin II was not affected. OPC-21268 may have clinical potentials in certain hypertensive cardiovascular disorders. In addition, an orally active and specific vasopressin V2 receptor antagonist, OPC-31260 was also reported. Oral administration of OPC-31260 inhibited antidiuretic action of arginine vasopressin. OPC-31260 is thought to be useful in the treatment of certain disorders, such as the syndrome of inappropriate secretion of ADH (SIADH).

Amino Acid Sequence↗
PubMed2004

Vasopressin and oxytocin in normal reproduction and in the pathophysiology of preterm labour and primary dysmenorrhoea. Development of receptor antagonists for therapeutic use in these conditions.

Vasopressin and oxytocin are synthesised in the hypothalamus and released to the blood stream via the posterior lobe of the hypophysis. Research during later years has shown that these peptides are also produced in other parts of the brain. The secretion to plasma is stimulated by oestrogen, an effect which is counteracted by progestagen. During delivery the fetus can also produce substantial amounts of vasopressin and oxytocin. Additionally, the uterus itself may be a source of these hormones and we have recently found oxytocin mRNA in the endometrium of non-pregnant women with the highest levels around the time of ovulation. In the onset of labour preterm and at term pregnancy vasopressin and oxytocin are centrally involved and in primary dysmenorrhoea the former hormone seems to play a key role in the mechanisms of increased contractions and reduced blood flow in the uterus of the condition. In women with the latter condition the plasma concentration of vasopressin is several-fold higher than that in healthy control persons. Both in pregnant and non-pregnant women the myometrium is activated via specific vasopressin V1a and oxytocin receptors. This vasopressin receptor is different from the vasopressin V1b receptor of the anterior lobe of the hypophysis, which is important in mood changes and V2 receptor of the kidneys mediating fluid reabsorption. At the onset of labour preterm and at term the vasopressin V1a and oxytocin receptors are elevated to a moderate degree. In non-pregnant women the receptor density varies over the menstrual cycle and increase markedly at the onset of menstruation. Substances, which block the uterine vasopressin V1a and oxytocin receptors inhibit preterm labour and primary dysmenorrhoea.

Antidiuretic Hormone Receptor Antagonists↗
PubMed1986

WRK1 cells: a model system for studying properties of V1a vasopressin receptors.

WRK1 cells, an established cell line derived from a chemically induced mammary tumor in the rat, are sensitive to vasopressin. Binding studies with intact WRK1 cells indicated the presence of a single population of [3H]vasopressin binding sites (dissociation constant, Kd = 12.7 +/- 0.2 nM, maximal binding capacity = 75 +/- 6 fmole/10(6) cells). Competition experiments using a series of vasopressin analogs with enhanced selectivity for the three subtypes of receptors already characterized--that is, renal V2 receptors, V1 receptors of the vascular or hepatic subtype (V1a), and V1 receptors from rat adenohypophysis (V1b)--indicated that vasopressin receptors from WRK1 cells have a ligand specificity very similar, if not identical, to that of V1a receptors. Vasopressin induced a marked (up to tenfold) increase in the production of labeled inositol phosphate (Ins 1,4,5 P3, Ins 1,4 P2, and Ins P) by WRK1 cells prelabeled with [3H]inositol. Antagonists of the vasopressor effect of vasopressin inhibited vasopressin-induced inositol lipid breakdown in WRK1 cells. For the entire series of vasopressin analogs tested, there was a close correlation between the respective Kd values for binding of these peptides to WRK1 cells and the corresponding Ka or Ki values derived from the determination of dose-dependent stimulation of inositol phosphate production, or inhibition of vasopressin-induced stimulation.

Animals↗
PubMed1989

Vasopressin receptors of the vasopressor (V1) type in the nucleus of the solitary tract of the rat mediate direct neuronal excitation.

The existence of vasopressin-sensitive neurons in the nucleus of the solitary tract of the rat and the presence in this brain area of vasopressin binding sites were investigated using extracellular single-unit recordings from brain-stem slices and light microscopic autoradiography. About 45% of the recorded neurons responded to vasopressin at 5-2000 nM by a reversible, concentration-dependent increase in firing rate. The action of vasopressin was direct, was suppressed by a vasopressor antagonist, and was mimicked by a vasopressor agonist. Oxytocin was 10-100 times less efficient than vasopressin and a specific antidiuretic agonist was without effect. Using light microscopic autoradiography and 3H-arginine vasopressin as a ligand, high-affinity vasopressin binding sites were found distributed over the whole rostrocaudal extent of the nucleus of the solitary tract. Binding was displaced by unlabeled vasopressor agonist but not by unlabeled antidiuretic agonist. Thus, the nucleus of the solitary tract contains V1-type vasopressin receptors which are, at least in part, located on neuronal membranes and whose activation generates bioelectrical signals. Solitary tract vasopressin-sensitive neurons may be the target of a vasopressinergic innervation originating in the hypothalamic paraventricular nucleus and could be involved in the central regulation of cardiovascular functions.

Animals↗