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PubMed2005

Arginine vasopressin as a rescue vasopressor agent in the operating room.

PURPOSE OF REVIEW: This review gives an overview of the current knowledge and research on the use of arginine vasopressin in cardiac arrest and severe shock states. RECENT FINDINGS: Animal models have revealed the effectiveness of arginine vasopressin in increasing vital organ perfusion during cardiopulmonary resuscitation. A multicentre trial compared arginine vasopressin and epinephrine in out-of-hospital cardiac arrest, and documented a significant improvement in hospital discharge rates in arginine vasopressin-treated (up to 2 x 40 IU) patients with asystole, and a significant benefit of the combined administration of arginine vasopressin and epinephrine on hospital discharge, irrespective of the underlying electrocardiographic rhythm. The stabilization of advanced shock states unresponsive to conventional therapy can be achieved by supplementary arginine vasopressin (1-4 IU/h). A randomized, controlled trial found that the combined infusion of arginine vasopressin and norepinephrine was superior to norepinephrine alone in reversing advanced vasodilatory shock. Furthermore, the successful employment of arginine vasopressin in uncontrolled haemorrhagic shock and other shock states, such as anaphylaxis, hypotension during spinal/epidural anaesthesia, postcardiotomy shock, acute brain injury, brain-dead organ donors, perioperative hypotension in patients chronically treated with angiotensin-converting enzyme inhibitors, shock after pheochromocytoma surgery, and carcinoid crisis have been reported. SUMMARY: Whereas arginine vasopressin in combination with epinephrine can significantly increase hospital discharge in cardiac arrest, arginine vasopressin combined with catecholamines improved haemodynamics in vasodilatory and haemorrhagic shock, but effects on outcome remain unknown. Nonetheless, in the perioperative setting, arginine vasopressin may already be considered as a potent adjunct vasopressor agent in advanced shock states unresponsive to conventional therapy.

Journal Article↗
PubMed1995

Vasopressin in the brain of a desert hibernator, the jerboa (Jaculus orientalis): presence of sexual dimorphism and seasonal variation.

The distribution of vasopressin innervation in the brain of the jerboa (Jaculus orientalis) was investigated, with special attention to sex differences and seasonal variations. Vasopressin perikarya were observed in the paraventricular and supraoptic nuclei, the suprachiasmatic nucleus, the periventricular nucleus, the medial preoptic area, the bed nucleus of the stria terminalis, and the medial amygdaloid nucleus. In addition, vasopressin cell bodies were observed in the ventral retrochiasmatic area. After treatment with colchicine, vasopressin perikarya were also observed around the organum vasculosum laminae terminalis, in the medial diagonal band of Broca, and in the dorsal medial preoptic nucleus. Vasopressin fibers were also found to be more widespread in the jerboa brain than in other rodents. Fibers were observed in the medial diagonal band of Broca, the stria medullaris, the tuber cinerum, the area postrema, the medial vestibular nucleus, and the dorsal motor nucleus of the vagus. Sexual dimorphism and seasonal variation in vasopressin immunoreactivity were observed in areas that not only showed a testosterone-dependent vasopressin innervation in other rodents but also in the paratenial and mediodorsal thalamic nuclei, the tuber cinerum, the supramammillary complex, the zona incerta, the interpeduncular complex, and the dorsal and medial raphe nuclei. A denser vasopressin innervation was observed in spring/summer (sexual active period) than in autumn. Numerous brain structures contained vasopressin receptors (cerebral cortex, hypothalamus, substantia nigra, dentate gyrus, thalamic nuclei, superior colliculus, dorsal cochlear nucleus, and cerebellum); no sex- or season-related differences were observed. These data indicate a high level of vasopressin in the jerboa brain, which may reflect an adaptation to its harsh bioclimatic environment.

Adaptation, Physiological↗
PubMed1989

Vasopressin rapidly stimulates protein kinase C in digitonin-permeabilized Swiss 3T3 cells: involvement of a pertussis toxin-insensitive guanine nucleotide binding protein.

Guanine nucleotides and pertussis toxin were used to test for the involvement of a guanine nucleotide binding protein in the vasopressin V1 receptor-mediated stimulation of protein kinase C activity in Swiss 3T3 cells. Addition of vasopressin in the presence of [gamma-32P]ATP and digitonin caused a marked and rapid increase (8 +/- 1-fold after 1 min) in the phosphorylation of an Mr = 80,000 cellular protein (80K), a specific marker for protein kinase C activation. This phosphorylation was selectively blocked by the V1 receptor antagonist Pmp1-0-Me-Tyr2 [Arg8] vasopressin, indicating that the effect was mediated through the vasopressin V1 receptor. Down regulation of protein kinase C by prior prolonged pretreatment of intact cells with phorbol 12,13-dibutyrate (PBt2) blocked the ability of vasopressin to stimulate the phosphorylation of 80K in digitonin-permeabilized cells. Addition of a submaximal concentration of vasopressin together with the GTP analogue GTP-gamma-S caused a synergistic stimulation of 80K phosphorylation. The GDP analogue GDP-beta-S caused a 50% inhibition of the phosphorylation of 80K induced by a saturating concentration of vasopressin and shifted the vasopressin dose-response curve to the right. GDP-beta-S had no effect on the dose-response for the stimulation of 80K phosphorylation induced by PBt2. Prior incubation of intact quiescent cultures of Swiss 3T3 cells with pertussis toxin did not impair either vasopressin-induced increase in cytosolic [Ca2+] or activation of protein kinase C. These findings provide functional evidence for the involvement of a pertussis toxin-insesitive G protein in the vasopressin V1 receptor-mediated stimulation of protein kinase C in Swiss 3T3 cells.

Animals↗
PubMed1994

Receptors for and myometrial responses to oxytocin and vasopressin in preterm and term human pregnancy: effects of the oxytocin antagonist atosiban.

OBJECTIVE: Our purpose was to study myometrial oxytocin and type V1 vasopressin receptors, the in vitro contractile effects of these hormones, and the influence of an oxytocin antagonist. STUDY DESIGN: Women delivered by cesarean section preterm (n = 51) and at term (n = 71), with and without labor contractions, gave myometrium for the estimation of oxytocin and V1 vasopressin receptors. The in vitro myometrial effects of the peptides and the influence on these of the competitive oxytocin receptor blocking agent 1-deamino-2-D-Tyr(OEt)-4-Thr-8-Orn-oxytocin were also tested. RESULTS: The median concentration of oxytocin receptors was 116 fmol/mg protein (range 15 to 372 fmol/mg protein) in patients delivered preterm not in labor, 134 fmol/mg protein (27 to 1421 fmol/mg protein) in the beginning of labor, and 46 fmol/mg protein (9 to 140 fmol/mg protein) in advanced labor. At term the corresponding concentrations were 172 (25 to 629), 223 (24 to 414), and 70 (21 to 92) fmol/mg protein. The concentration of V1 vasopressin receptors also decreased in advanced labor. In advanced labor after oxytocin infusion a reduction in the concentration of the receptor for this hormone was observed, which appeared to be related to the duration and dose of treatment. Oxytocin receptors did not vary between women with different indications for cesarean section. The oxytocin effects in vitro and the degree of inhibition by the antagonist of oxytocin responses correlated with the concentration of oxytocin receptors but not with that of V1 vasopressin receptors. No correlation was seen between the response to vasopressin and concentrations of oxytocin or V1 vasopressin receptors. CONCLUSIONS: The effect of oxytocin on the myometrium in pregnancy is mediated by an oxytocin receptor, whereas vasopressin acts on both oxytocin and vasopressin receptors. The initiation of labor both preterm and at term may be primarily related to increased release of oxytocin, which is locally produced in the uterus and not detectable in the plasma, but oxytocin and vasopressin receptors may play a role in the regulation of labor. The analog 1-deamino-2-D-Tyr(OEt)-4-Thr-8-Orn-oxytocin, which blocks both the oxytocin and the V1 vasopressin receptor, should inhibit labor both preterm and at term, the former confirming results of recent clinical studies in Sweden and the United States.

Cesarean Section↗
PubMed1992

Generation of anti-idiotypic monoclonal antibodies recognizing vasopressin receptors in cultured cells and kidney sections.

To produce anti-idiotypic antibodies against receptors for the neurohypophyseal hormone vasopressin, an anti-vasopressin monoclonal antibody with a ligand specificity similar to that of vasopressin receptors was employed for immunization. Three anti-idiotypic monoclonal antibodies were obtained which induced, like vasopressin, plasminogen activator production in the renal epithelial cell line LLC-PK1 (expressing V2-receptors). Induction of plasminogen activator synthesis by the anti-idiotypic antibodies could be inhibited by coincubation with a vasopressin antagonist. In a fashion similar to that of vasopressin itself, the anti-idiotypic antibodies induced receptor down-regulation. The anti-idiotypic antibodies were employed to visualize vasopressin receptors on LLC-PK1 and A7r5 (V1-receptor-expressing) smooth muscle cells by immunofluorescence. Antibody-mediated fluorescence was not observed in receptor-deficient mutant cell lines or vasopressin-receptor-down-regulated cells. Furthermore, 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.

Animals↗
PubMed2004

Comparative pharmacology of bovine, human and rat vasopressin receptor isoforms.

In this study, we characterized the bovine vasopressin V(1a), V(1b), V(2) receptor isoforms and compared their pharmacological properties to those of corresponding rat and human vasopressin receptor subtypes. Specific binding sites of high affinity for vasopressin were found in all bovine tissues tested (kidney, liver and pituitary). Using a large series of recent peptidic and non-peptidic selective vasopressin agonists or antagonists, we demonstrated the presence of vasopressin V(2), V(1a) or V(1b) receptors in the kidney, liver and pituitary bovine tissues, respectively. This extensive characterization of bovine vasopressin receptor isoforms validates the pharmacological vasopressin receptor classification earlier established for the rat and human species. As expected, the bovine vasopressin receptors look much more like human receptors than rat ones. Interestingly, among the three vasopressin receptor isoforms studied, the vasopressin V(1b) receptor subtype is the best conserved for the three species studied.

Animals↗
PubMed2000

Hypothalamic vasopressin gene expression increases in both males and females postpartum in a biparental rodent.

In previous studies, the closely related neuropeptide hormones oxytocin and vasopressin have been implicated in the central mediation of parental behaviour. Several studies in rats and sheep have demonstrated a role for oxytocin in the initiation of maternal behaviour. Recently, a few studies in a biparental species, the prairie vole (Microxytocinus ochrogaster) have suggested that vasopressin is important for paternal care. The present study investigated this latter possibility by measuring changes in vasopressin and oxytocin hypothalamic gene expression 1 day and 6 days following parturition in prairie voles which show paternal care and in montane voles (M. montanus) which lack paternal care. In prairie voles, vasopressin gene expression increased in both males and females postpartum, relative to sexually naive controls. In the non-paternal montane vole, no change in vasopressin gene expression was observed in either sex. In contrast to this species difference in vasopressin gene expression, hypothalamic oxytocin gene expression increased in both prairie and montane vole females, but not in males of either species. To augment measures of gene expression, we assessed vasopressin (V1a) and oxytocin receptor binding in both species. Although forebrain vasopressin V1a receptor binding was not altered following parturition in either species, oxytocin receptor binding increased in the ventromedial nucleus of the hypothalamus in females, but not males, in both prairie and montane voles. In summary, vasopressin gene expression increases in both males and females postpartum in a biparental species and oxytocin gene expression and receptor binding increase selectively in females. These results are consistent with earlier reports of a role for vasopressin in paternal care and for oxytocin in maternal behaviour.

Animals↗
PubMedDate not supplied

Migraine patients show increased platelet vasopressin receptors.

This study was designed to investigate vasopressin receptor status (Bmax and Kd) on platelets, vasopressin plasma levels, and vasopressin-induced platelet aggregation in migraine patients (21 females and 6 males) during a headache-free interval and in a matched control group. In the migraine group, Bmax was significantly higher (P = 0.02) at 53.9 +/- 20.6 fmol/mg than in the control group (36.8 +/- 21.0 fmol/mg). A correlation between Bmax and high or low sensitivity to vasopressin as an aggregator was evident in the control group, but not in the migraine group. No differences in Kd or in plasma levels of vasopressin between the migraine and control group were apparent. Men in both groups were much less sensitive to vasopressin as a platelet aggregator than were women (P < 0.01). Whether the higher Bmax in the migraine group is a reflection of temporarily higher vasopressin levels during headache or reflects a primary increase in sensitivity to vasopressin, remains to be clarified. The higher sensitivity of platelets (as a model for vessel wall receptors) from women may indicate why many more women than men suffer from migraine. Since the Bmax of the vasopressin receptor on platelets from migraine patients is increased compared to controls, treating migraine headache with vasopressin may deserve more attention.

Blood Platelets↗
PubMed2002

The role of arginine vasopressin in human labour: functional studies, fetal production and localisation of V1a receptor mRNA.

OBJECTIVE: To investigate labour-associated changes in: 1. the myometrial contractile response to arginine vasopressin compared with oxytocin in vitro 2. fetal production of arginine vasopressin and 3. myometrial vasopressin V1a receptor mRNA. DESIGN: The contractile response to vasopressin (compared with oxytocin) was investigated in paired myometrial strips in vitro. Blood was taken from the umbilical artery and vein at delivery and arginine vasopressin measured by radio-immunoassay. V1a receptor mRNA was determined by in situ hybridisation. RESULTS: Myometrium was more sensitive to arginine vasopressin than oxytocin (P<0.05 for frequency, amplitude and activity integral in paired strips) after, but not before labour. There was a marked umbilical arteriovenous difference in arginine vasopressin concentration at delivery suggesting fetal production which was not influenced by labour. Myometrial vasopressin V1a receptor mRNA was not increased after the onset of labour. CONCLUSIONS: The human uterus is extremely sensitive to arginine vasopressin in vitro. Arginine vasopressin is produced by the fetus but fetal formation is not increased during labour.

Adult↗
PubMed1989

Effect of the cessation of an infusion of vasopressin in acutely hypophysectomized anaesthetized dogs.

Stimulation of left atrial receptors in dogs anaesthetized with chloralose results in a reflex diuresis and a small decrease in the plasma concentration of vasopressin. It has been suggested that this diuretic response is solely mediated by the antidiuretic hormone, vasopressin (Gauer & Henry, 1976; Ledsome, 1985). The present investigation was designed to determine how these anaesthetized dogs, which are thought to be insensitive to changes in plasma vasopressin, respond to small decreases in plasma vasopressin similar to those observed during stimulation of left atrial receptors. In the event it was shown for the first time that it is possible to obtain a water diuresis in an anaesthetized animal in response to a small fall in the concentration of plasma vasopressin. In order to produce changes in plasma vasopressin similar to those seen during stimulation of left atrial receptors the pituitary gland was removed and an intravenous infusion of arginine vasopressin was given in eleven dogs anaesthetized with chloralose; a small decrease in plasma vasopressin was then produced by replacing the vasopressin with an infusion of saline for 30 min. A decrease in the plasma concentration of 1.29 pg cm-3 from a control concentration of 1.85 pg cm-3 resulted in a 96.7% increase in urine flow. The fall in concentration of vasopressin consequent upon stimulation of atrial receptors could, therefore, explain the water diuresis in the anaesthetized dog preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

Vasopressin: a regulator of adrenal glucocorticoid production?

Vasopressin infusion has been shown to decrease plasma adrenocorticotropic hormone (ACTH) concentration and transiently increase plasma cortisol concentration in conscious dogs. In the present study, one experiment tested the hypothesis that vasopressin infusion decreases ACTH by activation of a V1 receptor mechanism, e.g., by increasing atrial pressures and stimulating the low-pressure baroreceptor reflex. Administration of a vasopressin V1 antagonist eliminated the increases in atrial pressure and decreases in heart rate with vasopressin infusion (1 ng.kg-1.min-1), as it eliminated the decrease in ACTH, which is consistent with baroreflex-mediated inhibition of ACTH by vasopressin. A second experiment evaluated the role of ACTH in the increase in glucocorticoids. Dexamethasone pretreatment, which inhibits ACTH secretion, abolished the increase in glucocorticoid concentration with vasopressin infusion, indicating that ACTH is necessary for the glucocorticoid response. A third experiment was performed to determine whether the glucocorticoid response could be restored in dexamethasone-treated dogs, when ACTH concentration was maintained near control levels by intravenous infusion of synthetic alpha-ACTH-(1-24) (0.3 ng.kg-1.min-1). In these dogs, vasopressin infusion produced a sustained increase in plasma glucocorticoid concentration from 22 +/- 3 to 49 +/- 8 ng/ml (P less than 0.001). Infusing higher levels of ACTH (0.5 ng.kg-1.min-1) enhanced basal glucocorticoid levels but did not enhance the response to vasopressin. Vasopressin infusion did not alter clearance of glucocorticoids. Collectively, these results suggest that vasopressin directly stimulates adrenal glucocorticoid production, provided that background levels of ACTH are present.

Adrenal Glands↗
PubMed1982

Cardiac output distribution during vasopressin infusion or dehydration in conscious dogs.

To better understand the role of arginine vasopressin in cardiovascular regulation, we measured in unanesthetized dogs regional blood flows with radioactive microspheres before and during 1-h vasopressin infusions that increased the vasopressin concentration of plasma by 11 +/- 0.6 pg/ml. Cardiac output measured by an electromagnetic flowmeter decreased by 13%. Blood flows to the skeletal muscle and skin, the areas most affected, decreased by 30.8 and 34.3%, respectively. In the same group of dogs a period of 48-h water restriction increased plasma vasopressin by 6.9 +/- 1.3 pg/ml and reduced cardiac output by 14.4%. Skeletal muscle blood flow decreased by 32.8%, a pattern strikingly similar to that following vasopressin infusion. Obvious differences between vasopressin infusion and dehydration were also noted, in particular in the skin and splanchnic areas. However, the possibility that vasopressin contributed to the cardiovascular adjustments to dehydration must be considered. The use of an antagonist of the vascular effects of vasopressin, [1-deaminopenicillamine, 2-(O-methyl)tyrosine]arginine-vasopressin ([dPTyr(Me)]AVP), did not permit us to clarify this issue, because this analogue given alone exerted pronounced systemic and regional cardiovascular effects that resembled those of vasopressin.

Animals↗
PubMed1992

Reduced contractile sensitivity and vasopressin receptor affinity in DOCA-salt hypertension.

The affinity of vascular vasopressin receptors was studied to determine its role in altered vascular contractile sensitivity in deoxycorticosterone acetate (DOCA)-salt hypertension. Ring segments of rat mesenteric arteries were used to study vascular vasopressin receptors. Male Wistar rats were given subcutaneous injections of DOCA and 1% NaCl in the drinking water. Mesenteric arteries from hypertensive rats had a reduced contractile sensitivity to arginine vasopressin (AVP) and lysine vasopressin (LVP). The order of potency of vasopressin receptor agonists (AVP greater than LVP greater than oxytocin) was the same in arteries from hypertensive compared with normotensive animals. The affinity of the vasopressin receptor antagonist [deamino-Pen1,O-Me-Tyr2,Arg8] vasopressin, and the affinities of the vasopressin receptor agonists AVP and LVP were not altered during developing DOCA-salt hypertension. There was no change in contractile sensitivity to norepinephrine and KCl in arteries from hypertensive rats. The reduced vasopressin contractile sensitivity is not due to a change in vasopressin receptor affinity but may be a compensatory response to elevated blood pressure. These data suggest that increased vascular sensitivity does not contribute to elevated blood pressure during the developing stage of DOCA-salt hypertension.

Angiotensin Receptor Antagonists↗
PubMed2000

Renal vasopressin receptor expression and function in rats following spaceflight.

It has been suggested there is a decreased renal responsiveness to vasopressin following spaceflight and that this may be the mechanism for the increased urine flow that is observed following return to normal gravity. In the present study, we have therefore measured vasopressin receptor expression and activity in kidneys taken from rats 1 and 14 days following spaceflight of 15 days duration. Measurements of renal vasopressin V(2) and V(1a) receptor mRNA expression by quantitative RT-PCR demonstrated little difference at either 1 day or at 14 days following return from space. Evaluation of (3)H-labeled arginine vasopressin binding to membranes prepared from kidneys indicated that the majority of the vasopressin receptors were V(2) receptors. Furthermore, the data suggested that binding to vasopressin V(2) or V(1a) receptors was unaltered at 1 day and 14 days following spaceflight. Similarly, the ability of vasopressin to stimulate adenylate cyclase suggested no change in vasopressin V(2) receptor activity in these animals. These data suggest that, whatever changes in fluid and electrolyte metabolism are observed following spaceflight, they are not mediated by changes in vasopressin receptor number or vasopressin-induced stimulation of adenylate cyclase.

Animals↗
PubMed1994

Vasopressin mediates hypoglycemia-induced inhibition of luteinizing hormone secretion in the ovariectomized rhesus monkey.

The objective of the present study was to examine the role of vasopressin in the regulation of LH secretion in the rhesus monkey. The effect of vasopressin administration on basal LH secretion and vasopressin antagonism on stress-induced inhibition of LH secretion were examined. Intracerebroventricular (i.c.v.) infusion of vasopressin (20 micrograms/h) to chair restrained ovariectomized rhesus monkeys (n = 5) decreased the area under the LH curve by -51.61 +/- 13.73 ng/ml/h compared to -8.35 +/- 7.11 ng/ml/h following infusion of artificial CSF (aCSF; p = 0.021). This effect was independent of any change in mean arterial pressure. Subsequently, the role of vasopressin in hypoglycemia-induced suppression of LH was examined. Administration of insulin (1 U/kg BW) to chair-restrained ovariectomized rhesus monkeys decreased the area under the LH curve by -60.88 +/- 19.77 ng/ml/h. The decrease in LH was significantly different from that observed in aCSF-infused euglycemic controls which exhibited a slight decrease in LH (-8.35 +/- 7.11 ng/ml/h; p = 0.036). In contrast, the area under the LH curve was increased slightly (1.42 +/- 11.93 ng/ml/h) when insulin administration was combined with i.c.v. infusion of the vasopressin antagonist [deaminopenicillamine1, O-methyl-tyrosine2, arginine8]-vasopressin (120 micrograms/h; p = 0.013 vs. insulin only). The demonstration that vasopressin administration inhibits LH secretion whereas vasopressin antagonism prevents hypoglycemia-induced LH suppression suggests that vasopressin is a physiological inhibitor of LH secretion in the rhesus monkey.

Animals↗
PubMed1992

Different guanosine triphosphate-binding proteins couple vasopressin receptor to phospholipase C and phospholipase A2 in glomerular mesangial cells.

To evaluate the identity of the guanosine triphosphate--binding proteins coupling arginine vasopressin receptor occupancy with activation of phospholipase C, leading to Ca2+ mobilization, and activation of phospholipase A2, leading to arachidonate release and prostanoid formation, we used intact cells, saponin-permeabilized cells, and membranes of the rat mesangial cell. Arginine vasopressin 10(-7) mol/L produced a dose-dependent increase in cytosolic Ca2+ to maximal levels of 500 nmol/L with peak responses occurring within 10 seconds of addition of arginine vasopressin to cells in suspension. Arginine vasopressin 10(-7) mol/L elicited a maximal response. These increases were associated temporarily with a fourfold increase in tritiated D-myo-inositol 1,4,5-trisphosphate formation in prelabeled cells. Pertussis toxin (200 ng/ml) did not inhibit the Ca2+ increase nor did it inhibit the increase in tritiated D-myo-inositol 1,4,5-trisphosphate formation, suggesting a pertussis toxin--insensitive signaling pathway for phospholipase C hydrolysis in response to vasopressin. Membranes prepared from mesangial cells increased D-myo-inositol 1,4,5-trisphosphate formation in vitro in response to arginine vasopressin and guanosine-5'-0(3- thiotrisphosphate), and this stimulation was inhibited by guanosine-5'-0(2-thiodiphosphate), confirming the involvement of a guanosine triphosphate--binding protein. In contrast arginine vasopressin stimulated arachidonate release from intact mesangial cells, and this effect was blocked by pretreating cells with pertussis toxin. To demonstrate that this was through a pertussis toxin--sensitive guanosine triphosphate--binding protein, we permeabilized cells with saponin and determined that arginine vasopressin and guanosine-5'-0(3-thiotriphosphate) stimulated the release of arachidonic acid and the stimulation of guanosine-5'-0(3-thiotriphosphate) was inhibited by guanosine-5'-0(2-thiodiphosphate). Finally, pertussis toxin was able to stimulate adenosine diphosphate ribosylation in vivo of a substrate protein in mesangial cell membranes of 41 kd, and this ribosylation was inhibited by pretreating cells with pertussis toxin. These data suggest that the release of arachidonic acid by vasopressin in glomerular mesangial cells is linked to a pertussis toxin--sensitive guanosine triphosphate--binding protein and that this activation of phospholipase C in vasopressin is linked to a pertussis toxin--insensitive guanosine triphosphate--binding protein.

Adenosine Diphosphate Ribose↗
PubMed1987

Noncompetitive blockade of vasopressin-1 receptors in rat tail artery.

To study vasopressin-1 receptor-mediated contraction of the isolated rat tail artery, pseudoirreversible blockade was produced by incubating tissues with 10 nM 1-beta-mercapto,beta,beta,cyclopentamethylene propionic acid, 2(O-me)tyrosine,-8-D-arginine vasopressin and 1.2 mM magnesium. Concentration-response curves to vasopressin agonists were constructed before and during exposure to 1-beta-mercapto,beta,beta,cyclopentamethylene propionic acid, 2(O-me)tyrosine,-8-D-arginine vasopressin, and at three time points after washing out the antagonist. EC50 values (-log M) for arg-vasopressin (AVP, 8.02 +/- 0.16) and arg-vasotocin (AVT, 9.51 +/- 0.12) were unaltered after exposure to the antagonist and washing of the tissues. The control EC50 for lys-vasopressin (LVP, 8.33 +/- 0.09) was significantly lower than after blockade (P less than .05). At each time point after blockade, the intrinsic activity of LVP was greater than either AVP or AVT. Increasing the ambient magnesium ion concentration greater than 1.2 mM did not alter responses to vasopressin agonists. Reducing the ambient magnesium ion from 1.2 mM to zero increased the EC50 values for all vasopressin agonists by 6- to 20-fold, but had no effect on maximal response size, nor on the concentration-response curve for norepinephrine. Pseudoirreversible blockade performed in the absence of magnesium also increased the EC50 for LVP but not for AVP or AVT after exposure to the antagonist. We conclude that LVP has greater efficacy than AVP and AVT at vasopressin receptors in rat tail artery, and that magnesium ions affect only agonist affinity but not efficacy at this vasopressin-1 receptor.

Animals↗
PubMed1985

Internalization, recycling, and redistribution of vasopressin receptors in rat hepatocytes.

Three hours after isolation, cultured hepatocytes have approximately 150,000 surface vasopressin receptors/cell, and these exhibit a Kd for 125I-vasopressin of 6 nM based on calculation of Koff/Kon, or a Kd of 9.5 nM based on Scatchard plot analysis. After the binding of 125I-vasopressin to its receptor on the hepatocyte surface, this complex is internalized with a t1/2 of 3-6 min. Following this internalization, the number of vasopressin receptors on the cell surface is restored both in vitro and in the isolated perfused liver with a t1/2 of 8-10 min. This restoration is blocked in vitro by incubation of the hepatocytes at 18 degrees C, but not by cycloheximide, suggesting that internalized vasopressin receptors recycle back to the cell surface. Prolonged incubation of hepatocytes with vasopressin results in the loss of greater than 75% of the vasopressin surface binding at concentrations of vasopressin approximately equivalent to its Kd. The binding of vasopressin to cultured hepatocytes 3-5 h after isolation resembles binding to the isolated perfused whole liver with respect to receptor dynamics. During culture for 48 h, however, we observe a progressive loss of hepatocyte surface vasopressin receptors. Concomitant with this reduction in surface receptors with time in culture, there appears to be a marked elevation in intracellular receptors.

Animals↗