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PubMed1997

Proconvulsive effect of vasopressin; mediation by a putative V2 receptor subtype in the central nervous system.

Subcutaneously (s.c.) administered [Arg8]vasopressin (AVP) potentiated seizures induced by intracerebroventricular (i.c.v.) injection of 1.95 mg pilocarpine (a muscarinic cholinergic agonist). A bell-shaped relation between dose and effect was found. I.c.v. pretreatment with a V1, V2 or oxytocin receptor antagonist was performed to determine whether and what type of receptor is involved in this proconvulsive effect of vasopressin. For these experiments a higher dose of pilocarpine (2.4 mg i.c.v.) was injected. This caused seizures in a slightly but not significantly higher percentage of the rats. A dose-dependent protective action of the V2 receptor antagonist d(CH2),[D-Ile2,Ile4]AVP (effective doses were 25 and 125 ng) on seizures was found. A reduction was observed in the number of animals that developed tonic-clonic convulsions. Neither the V1 receptor antagonist d(CH2)5[Tyr(Me)2]AVP nor the oxytocin receptor antagonist desGly(NH2)9d(CH2)5[Tyr(Me)2Thr4]OVT possessed anti-convulsive activity. Subsequently the type of receptor was studied in detail with fragments of AVP with either V1 or V2 activity. AVP (with V1 and V2 affinity) (1 and 3 microg s.c.) potentiated pilocarpine (1.95 mg) induced seizures. Vasotocin and oxytocin were without effect. Interestingly neither s.c. nor i.c.v. administration of the selective kidney type vasopressin receptor (V2) agonist dDAVP potentiated pilocarpine induced seizures. Several selective antidiuretic agonists (V2), such as d[Val4]AVP, d[Phe2,Val4,D-Arg8]vasopressin (3 microg), [Val4,D-Arg8]vasopressin (3 microg) and d[Val4,D-Arg8]vasopressin (3 microg) were active. Other selective antidiuretic compounds, such as [Val4]AVP, dAVP, d[Tyr(Me)2]AVP and HO[D-Arg8]vasopressin (3 microg) did not influence seizures. These results demonstrate that a combination of substitution of aminoacid 4 (Gln) by Val and to a lesser extent deamination and the D-arginine form yield an active molecule, which can potentiate pilocarpine induced seizures and suggest the existence of a V2 receptor subtype in the brain.

Animals↗
PubMed1998

Potentiation of receptor-mediated cAMP production: role in the cross-talk between vasopressin V1a and V2 receptor transduction pathways.

Cross-talk between the phospholipase C and adenylyl cyclase signalling pathways was investigated in Chinese hamster ovary (CHO) cells transfected with the V1a and V2 vasopressin receptors. Cell lines expressing V1a, V2, or both V1a and V2 receptors, were established and characterized. Stimulation of V2 receptors by vasopressin induced a dose-dependent increase in cAMP accumulation, whereas stimulation of V1a receptor resulted in an increase in intracellular calcium without any change in basal cAMP. The simultaneous stimulation of V2 and V1a receptors by vasopressin elicited an intracellular cAMP accumulation which was twice that induced by stimulation of V2 receptor alone with deamino-[d-Arg8]vasopressin. This potentiation between V1a and V2 receptors was mimicked by activation of protein kinase C (PKC) with PMA, and was suppressed when PKC activity was inhibited by bisindolylmaleimide. The potentiation was observed in the presence or absence of 1 mM 3-isobutyl-1-methylxanthine, a phosphodiesterase inhibitor, implying that an alteration in cAMP hydrolysis was not involved. Vasopressin, as well as PMA, had no effect on the forskolin-induced cAMP accumulation, suggesting that PKC did not directly stimulate the cyclase activity. On the other hand, vasopressin, like PMA, potentiated the cAMP accumulation induced by cholera toxin, an activator of Galphas protein. These results suggest that, in CHO cells, vasopressin V1a receptor potentiates the cAMP accumulation induced by the V2 receptor through a PKC-dependent increase in the coupling between Gs protein and adenylyl cyclase.

1-Methyl-3-isobutylxanthine↗
PubMed1981

A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria.

The diagnoses provided by a standard indirect test of vasopressin function were compared with those obtained by radioimmunoassay of plasma vasopressin in 24 patients with nonglucosuric polyuria. All seven cases of severe neurogenic diabetes insipidus diagnosed by the indirect tests were confirmed by the vasopressin assay. However, two of six patients with partial neurogenic diabetes insipidus by indirect criteria had normal vasopressin secretion by the direct assay; one was found to have primary polydipsia, and the other nephrogenic diabetes insipidus. Moreover, three of 10 patients diagnosed as having primary polydipsia by the indirect test had clear evidence of partial vasopressin deficiency by the direct assay. The inability of the indirect test to distinguish accurately between partial neurogenic diabetes insipidus and primary polydipsia may be explained by increased sensitivity to low concentrations of vasopressin in the former disorder and a reduction of maximal concentrating ability in both. We conclude that the incorporation of a vasopressin assay improves accuracy in the differential diagnosis of polyuria.

Adolescent↗
PubMed2003

Vasopressin increases urinary albumin excretion in rats and humans: involvement of V2 receptors and the renin-angiotensin system.

BACKGROUND: An increase in urinary albumin excretion (UAE) represents an early predictor of glomerular damage in diabetes mellitus (DM) and a risk factor for cardiovascular complications in hypertension. Vasopressin is elevated in DM and in some forms of hypertension. Previous studies in rats suggested that this hormone could play a role in the albuminuria observed in chronic renal failure or diabetic nephropathy, but no information is available concerning the mechanism of these effects and the possible influence of vasopressin on UAE in the healthy kidney. The present study was thus designed to evaluate whether vasopressin influences UAE in normal rats and humans, whether this effect is V(2)-receptor-dependent, and whether it is mediated by the renin-angiotensin system. METHODS: UAE was measured in normal Wistar rats and healthy humans, or in subjects with various forms of diabetes insipidus (DI), before and after acute or chronic infusion of the vasopressin V(2) receptor agonist dDAVP. Chronic dDAVP administration was also performed in normal Wistar rats previously submitted to either chronic angiotensin-converting enzyme inhibition (ACEI) or chronic blockade of AT1 receptors (ARB). RESULTS: In rats, acute or chronic dDAVP infusion increased UAE significantly and reversibly (4-fold and 6-fold, respectively). In healthy subjects, acute infusion of dDAVP tripled UAE (P<0.01) but did not change creatinine and beta(2)-microglobulin excretion, thus suggesting that the rise in UAE was due to an increased glomerular leakage of albumin. dDAVP also increased UAE in patients with central DI and in patients with hereditary nephrogenic DI bearing AQP2 mutations. However, UAE was not increased in patients with hereditary nephrogenic DI bearing mutations of the V(2) receptor. In rats, ACEI and ARB blunted the dDAVP-induced rise in UAE by 70% (P<0.05) and 50% (NS), respectively. CONCLUSIONS: The present studies reveal for the first time that vasopressin induces a marked increase in UAE in healthy rats and humans. This albuminuric effect seems to result from increased glomerular leakage, requires functional vasopressin V(2) receptors, and is, at least in part, mediated by the renin-angiotensin system. These results bring additional support for an involvement of vasopressin in the albuminuria observed in pathological states such as diabetes mellitus or hypertension.

Adult↗
PubMed1986

A V1 vasopressin receptor antagonist has nonspecific neurodepressant actions in the spinal cord.

In the present investigation, we injected d(CH2)5Tyr(Me)AVP, a specific VI vasopressin antagonist, into the intrathecal space of the spinal cord to determine whether spinal vasopressin-containing neurons contribute to the hemodynamic effects produced by stimulation of the paraventricular nucleus (PVN). The intrathecal antagonist reduced the cardiovascular effects of PVN stimulation, but also reduced the effects produced by stimulating 2 other brain sites which do not contain vasopressin cell bodies. In addition, intrathecal administration of the vasopressin antagonist had a similar effect in Brattleboro rats which do not produce vasopressin. In conscious rats with indwelling intrathecal catheters, the vasopressin antagonist produced reversible hindlimb paralysis. These data suggest that d(CH2)5Tyr(Me)AVP has nonspecific actions within the spinal cord not related to the blockade of vasopressin receptors.

Animals↗
PubMed1992

Hydroosmotic activities of arginine-vasopressins modified either in positions 1, 2 and 4 or at N-terminal extensions.

Vasopressin and its synthetic analogs were studied for their effect on transepithelial water flux in frog urinary bladder. As compared with AVP, 1-deamino-8-D-arginine vasopressin (dDAVP) was about 40 times less effective in stimulating osmotic water flow. The vasopressin analogs obtained by modification in positions 1 and 2 were: [1-(1-mercapto-4-tert-butylcyclohexaneacetic acid)] AVP (I); [1-(1-mercapto-4-methylcyclohexaneacetic acid)]AVP (II); [1-(1-mercapto-4-methylcyclohexaneacetic acid)-2-O-methyltyrosine]AVP (III); and those modified in position 4 were: [1-(1-mercaptocyclohexaneacetic acid)-4-arginine] AVP (IV); [1-(2-mercaptopropionic acid)-4-arginine]AVP (V). Any of the above analogs did not influence basal, but antagonized vasopressin-stimulated water flux. N-terminally extended analogs of AVP: Ala-AVP (VI); Ser-Ala-AVP (VII) and Thr-Ser-Ala-AVP (VIII) stimulated osmotic water flux to the same extent in concentration 200 times higher as that of AVP. We conclude from these studies that vasopressin analogs (I-V) competitively antagonize vasopressin-stimulated hydroosmotic activity in frog urinary bladder probably at the epithelial vasotocin V1 and/or V2 receptor site. N-terminal extension of the vasopressin molecule did not influence the capacity of AVP to induce V2 receptor-mediated action, even when used at higher concentrations.

Amino Acid Sequence↗
PubMed2001

Cardiovascular regulation of vasopressin neurons in the supraoptic nucleus.

This paper reviews the regulation of hypothalamic vasopressin and oxytocin neurosecretory cells in the neural response to plasma volume expansion. Many questions remain unanswered regarding how an increase in volume affects neurohypophysial hormone secretion, what receptors are important in mediating this response, and which neural pathways are responsible for conveying the signal from those receptors to the hypothalamus. Plasma volume expansion activates regions of the central nervous system associated with inhibition of vasopressin release, oxytocin secretion, and inhibition of sympathetic nerve activity. Cardiac receptors, not arterial baroreceptors, are primarily responsible for activation of the regions associated with regulation of vasopressin secretion and sympathetic outflow. Other stimuli that as yet are undefined account for activation of oxytocin-secreting neurons. Electrophysiology experiments have measured the inhibition of vasopressin-secreting magnocellular neurons in the supraoptic nucleus by select stimulation of cardiac receptors in the caval-atrial junction. Further experiments suggest that the perinuclear zone, a population of neurons surrounding the supraoptic nucleus, is a necessary part of the pathway by which caval-atrial stretch decreases the excitability of vasopressin neurons. The perinuclear zone is also a necessary synapse for arterial baroreceptor-mediated inhibition of vasopressin neurons. This suggests that the neural pathways that inhibit vasopressin release in response to an increase in blood pressure and an increase in blood volume may overlap at the perinuclear zone of the supraoptic nucleus. Finally, the integration of various neural pathways activated by multiple receptors to ultimately determine the activity of magnocellular neurons and vasopressin secretion is discussed.

Animals↗
PubMed2004

Vasopressin.

Vasopressin is a hormone that is essential for both osmotic and cardiovascular homeostasis. A deficiency of vasopressin exists in some shock states and replacement of physiological levels of vasopressin can restore vascular tone. Vasopressin is therefore emerging as a rational therapy for vasodilatory shock. In this article we review the rationale and summarize the evidence for using vasopressin in vasodilatory shock states, such as septic shock. We then highlight the areas of uncertainty in using vasopressin for septic shock and summarize the reasons for clinical equipoise. We close by suggesting that further randomized controlled trials of vasopressin in septic shock are required before vasopressin is used routinely for management of septic shock.

Journal Article↗
PubMed2002

Arginine vasopressin during cardiopulmonary resuscitation: laboratory evidence, clinical experience and recommendations, and a view to the future.

When stimulating adult pigs with ventricular fibrillation or postcountershock pulseless electrical activity for cardiopulmonary resuscitation, vasopressin improved vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery better than epinephrine. In pediatric preparations with asphyxia, epinephrine was superior to vasopressin, whereas in both pediatric pigs with ventricular fibrillation and adult porcine models with asphyxia, combinations of vasopressin and epinephrine proved to be highly effective. This may suggest that a different efficiency of vasopressors in pediatric vs. adult preparations and different effects of dysrhythmic vs. asphyxial cardiac arrest on vasopressor efficiency may be of significant importance. Whether these theories can be extrapolated to humans is unknown at this time. In patients who experienced out-of-hospital ventricular fibrillation, a larger proportion of patients treated with vasopressin survived 24 hrs compared with patients treated with epinephrine; during in-hospital cardiopulmonary resuscitation, comparable short-term survival was found in groups treated with either vasopressin or epinephrine. Currently, a large trial comprising patients who experience out-of-hospital cardiac arrest and who are treated with vasopressin vs. epinephrine is ongoing in Germany, Austria, and Switzerland. The new cardiopulmonary resuscitation guidelines of both the American Heart Association and the European Resuscitation Council consider 40 units of vasopressin intravenously and 1 mg of epinephrine intravenously equally effective for the treatment of adult patients with ventricular fibrillation; however, because of a lack of clinical data, no recommendation for vasopressin has been made for adult patients with asystole and pulseless electrical activity or for pediatric patients.

Adult↗
PubMed1993

Potentiation of the classic ovine corticotrophin releasing hormone stimulation test by the combined administration of small doses of lysine vasopressin.

OBJECTIVE: To assess the corticotrophic response to ovine corticotrophin releasing hormone (CRH) with the lowest dose of lysine vasopressin able to induce both the greatest stimulation and the lowest degree of side-effects. SUBJECTS: Fourteen healthy young adult males. DESIGN: Increasing intravenous doses (either 0, 0.03, 0.1, 0.3, or 1 IU) of lysine vasopressin, infused over 20 minutes, combined with a bolus of 100 micrograms ovine CRH. MEASUREMENT: Radioimmunoassay of plasma ACTH, lipotrophin hormones and cortisol levels. RESULTS: (1) Responses to stimulation tests were evaluated as the area under the curves of plasma levels versus sample times, from 0 to 120 minutes after injection or start of perfusion (six subjects). The lowest dose of lysine vasopressin that induced an additional stimulation in the CRH-stimulated ACTH response was 0.3 IU. The combination of 1 IU lysine vasopressin with CRH doubled values of the area under the curve for the ACTH. Lysine vasopressin alone (0.3 and 1 IU) failed to stimulate ACTH responses. (2) The combined test (100 micrograms CRH and 1 IU lysine vasopressin) was carried out on eight additional control subjects. From a mean basal level of 23 +/- 5.6 (SEM), plasma ACTH peaked to 104.5 +/- 8 ng/l (23.0 +/- 1.8 pmol/l) as early as 20-30 minutes after the start of injection. When repeated after a two-week interval, the combined test induced identical stimulation in a given subject. Results of lipotrophin hormone determinations roughly paralleled those of ACTH. However the effects on cortisol levels were less clear. Subjects injected with CRH experienced slight facial flush. Following the 1 IU lysine vasopressin dosage, side-effects were reduced to skin pallor. No changes in heart-rate or blood-pressure were observed. CONCLUSIONS: Under these conditions, the combination of 100 micrograms CRH with 1 IU lysine vasopressin constitutes a powerful test for direct assessment of the pituitary reserve and therefore can be employed as a routine investigational tool.

Adrenocorticotropic Hormone↗
PubMed1986

Vasopressin induced myocardial depression in neurally mediated and not due to impaired coronary blood flow.

The mechanism of the cardiodepressant effect of vasopressin was studied by measuring simultaneously myocardial contractile force and coronary blood flow (with tracer microspheres) in anaesthetized open-chest rabbits. Lysine-vasopressin administered at two dose levels (10 and 100 mu kg-1 infused in 2 min with a maintenance dose of 2 mu kg-1 min-1 between these two loading doses) to a group of 6 rabbits caused dose-dependent myocardial depression and also severely decreased coronary blood flow in a dose-dependent manner. Blood pressure remained almost unchanged but heart rate, cardiac output and total peripheral conductance were also decreased dose-dependently. In another group of 6 rabbits treated in the same way with lysine-vasopressin, darodipine (PY 108-068, 30 and 100 micrograms kg-1) was infused intravenously. It reversed the vasopressin-induced coronary constriction and cardiodepression. The high dose of vasopressin brought back cardiac depression but did not reduce coronary blood flow below baseline values. Myocardial depression could therefore not be adequately explained by the changes in coronary blood flow. In a further group of rabbits which had been subjected to cervical vagotomy and beta-adrenoceptor blockade (propranolol 1 mg kg-1 i.v.) before the experiment, vasopressin still caused coronary constriction which was reversed by darodipine, but had no effect on myocardial contractile force and heart rate. The cardiodepressant effect of vasopressin can thus be explained fully by effects on the autonomic nervous system which are reversed by lowering blood pressure, whereas the severe reduction of coronary flow did not contribute to the vasopressin-induced myocardial depression.

Animals↗
PubMed1987

Adrenergic mediation of vasopressin secretion in newborn pigs.

Effects of inhibition of alpha 1-(prazosin) and alpha 2-(yohimbine) adrenoreceptors on plasma lysine vasopressin concentration during normotension and hemorrhagic hypotension were studied in unanesthetized newborn pigs. During the normotensive period, treatment with prazosin and yohimbine both increased plasma lysine vasopressin concentration (vehicle = 3.4 +/- 1.21 microU/ml; prazosin = 35.8 +/- 10.8 microU/ml; and yohimbine = 20.1 +/- 9.5 microU/ml). Prazosin caused a decline in arterial pressure (vehicle = 60 +/- 6 mmHg; prazosin = 49 +/- 5 mmHg), which may account for the increase in plasma lysine vasopressin concentration, whereas yohimbine increased arterial pressure (73 +/- 3 mmHg). On hemorrhage to equivalent arterial pressure, plasma lysine vasopressin concentration increased to similar levels in vehicle- (110.3 +/- 28.7 microU/ml) and prazosin-treated (92.6 +/- 14.2 microU/ml) piglets. In contrast, on hemorrhage of yohimbine-treated piglets, the increase in plasma lysine vasopressin concentration was augmented remarkably (527.0 +/- 103.2 microU/ml) in comparison to the other groups. We conclude that, in unanesthetized newborn pigs, treatment with the alpha 2-adrenoreceptor antagonist yohimbine increased plasma lysine vasopressin concentration and markedly accentuated the vasopressin response to hemorrhage. An alpha 2-adrenergic receptor-mediated mechanism appears to be an important inhibitory component in the vasopressin secretory system of the newborn pig.

Animals↗
PubMed1994

Vasopressin-induced neurotrophism in cultured hippocampal neurons via V1 receptor activation.

Structural enhancement of nerve cell morphology has been postulated to be an integral step in the cellular process leading to information storage in the nervous system. To investigate this postulate, we determined whether vasopressin (AVP), a neural peptide that can enhance memory function, would enhance the cytoarchitectural features of hippocampal neurons in culture. Results of these studies demonstrated that in the presence of serum, vasopressin (1 microM), induced a significant increase in the number of neurites, in neuritic length, and in neurite diameter following 48 h of exposure. Morphological complexity was also enhanced following vasopressin exposure as indicated by a significant increase in the number of filopodia/branches, in the sum of branch lengths, and in the number of branch bifurcation points. The number of microspikes decorating neuritic branches was also significantly increased following vasopressin exposure. To determine whether the neurotrophic effect of vasopressin was dependent upon factors present in serum, hippocampal nerve cells were cultured in serum-free media and exposed to 100-1000 nM AVP. Results of these studies demonstrated that in the absence of serum, AVP induced significant enhancement of hippocampal nerve cell growth and that the minimally effective concentration was reduced from 1 microM, as required in the presence serum, to 100 nM. In addition, the time required for a significant increase in nerve cell growth to become apparent decreased from 48 to 24 h. These results demonstrate that AVP-induced neurotrophism is not dependent upon unidentified factors in serum. AVP-induced neurotrophism was found to be mediated by V1 receptor activation. Significant enhancement of nerve cell growth occurred following exposure to V1 receptor agonist (100-1000 nM), whereas exposure to V2 receptor agonist (100-1000 nM) did not increase any of the morphological parameters measured. Considered together, these data indicate that vasopressin can exert a significant neurotrophic effect upon hippocampal nerve cells in culture. Moreover, AVP-induced neurotrophism is a direct effect and not dependent upon unidentified factors present in serum. Enhancement of hippocampal nerve cell growth occurred in the presence of a specific V1 receptor agonist and not following exposure to a V2 agonist, suggesting that activation of the phosphatidyl inositol pathway via V1 receptor activation mediates AVP-induced neurotrophism. Results of these studies are discussed with respect to their implications for understanding vasopressin involvement during neural development and induction of cytoarchitectural modifications associated with memory formation.

Animals↗
PubMed2001

High concentrations of oxytocin cause vasoconstriction by activating vasopressin V1A receptors in the isolated perfused rat kidney.

The aim of this study was to evaluate the renal vascular effects of oxytocin in Sprague-Dawley rats and in Brattleboro heterozygous or homozygous rats, the latter being genetically deficient in vasopressin synthesis. Studies were performed in vitro, in the isolated kidney perfused in an open circuit with a Tyrode's solution. Oxytocin induced a concentration-dependent renal vasoconstriction in Sprague-Dawley rats, at rather high concentrations (EC50=170+/-39 nM, mean +/- SEM, n=6) with a maximum response amounting to 44% of that elicited by vasopressin (increase in renal vascular resistance: 11.5+/-0.9 mmHg min ml(-1) vs. 26.2+/-2.2 mmHg min ml(-1)). Oxytocin-evoked renal vasoconstriction was abolished by SR 49059, a selective vasopressin V1A receptor antagonist (10 nM), but not by d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-(NH2)9] vasotocin, an oxytocin receptor antagonist (10 nM). In the presence of SR 49059, oxytocin did not induce renal vasorelaxation. Oxytocin induced renal vasoconstriction in Brattleboro homozygotes and heterozygotes (EC50=59+/-12 nM and 262+/-110 nM; Emax=7.8+/-1.1 mmHg min ml(-1) and 6.9+/-0.4 mmHg min ml(-1), n=5 respectively) with characteristics similar as observed in Sprague-Dawley rats concerning partial agonist activity, low potency and antagonism by SR 49059. Responsiveness to vasopressin did not differ in Brattleboro homozygotes and heterozygotes (EC50 approximately 0.25 nM) and was similar as we reported in Sprague-Dawley rats. These findings indicate that high concentrations of oxytocin induce renal vasoconstriction in the rat by activating vasopressin V1A receptors. The low agonist activity makes it unlikely that oxytocin can substitute functionally for vasopressin at the renal vascular V1A receptor in Brattleboro homozygous rats which are deficient in endogenous vasopressin.

Animals↗
PubMed1976

Plasma arginine vasopressin in the syndrome of antidiuretic hormone excess associated with bronchogenic carcinoma.

A study of plasma arginine vasopressin in 17 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with bronchogenic carcinoma, revealed that the arginine vasopressin levels were distinctly elevated in most. In 14 patients with bronchogenic carcinoma, but without overt SIADH, plasma levels of arginine vasopressin were significantly higher than in normal subjects (p less than 0.001). This, together with the finding of a lower than normal plasma osmolality in this group, suggests that inappropriate ADH excess might be much more common in patients with bronchogenic carcinoma than previously thought. The normal positive correlation between plasma osmolality and plasma arginine vasopressin was found to be reversed in SIADH. Seven of nine patients with overt SIADH, studied after fluid deprivation, showed an increase in plasma arginine vasopressin coincident with an increase in plasma osmolality (r = +0.8, p less than 0.01); in one patient, plasma arginine vasopressin returned to the original level following rehydration. The possibility that this might imply a degree of physiologic control to what is generally considered an autonomous secretion is discussed. It is, however, considered more likely that other factors, including changes in plasma volume and glomerular filtration, might explain the increase in plasma levels of arginine vasopressin.

Adult↗
PubMed1991

Expression of vasopressin V2 receptor in Xenopus laevis oocytes by porcine kidney cell line (LLC-PK1) messenger RNA.

Vasopressin V2 receptor was expressed in Xenopus laevis oocytes which were injected with poly(A) +RNA from porcine kidney cell line LLC-PK1. Pharmacological antagonism of the expressed V2 receptor was observed between arginine vasopressin and two potent and selective vasopressin antagonists: [d(CH2)5, D2-Phe2 Ile4, Ala9-NH2]arginine vasopressin and [d(CH2)5,D-Ile2, Ile4]arginine vasopressin. Activation constant for arginine vasopressin concentration was 1.32 x 10(-10)M. The nucleotide length of the mRNA encoding for vasopressin V2 receptor was deduced to be approximately 2 kilobases.

Adenylyl Cyclases↗
PubMed1986

Interrelationship between central bradykinin and vasopressin in conscious rats.

Intracerebroventricular administration of bradykinin (1, 5 and 20 micrograms) into conscious rats resulted in significant dose-dependent increases in the plasma vasopressin concentration, mean arterial blood pressure and heart rate. Peripheral blockade of the pressor action of vasopressin with a vasopressin pressor antagonist (10 micrograms/kg, i.v.) did not cause an attenuation but rather a potentiation and prolongation of the pressor effects of central bradykinin (20 micrograms). Central administration of the vasopressin antagonist (150 ng) caused no peripheral blockade of the pressor effects of exogenous i.v. vasopressin but almost abolished the bradykinin-induced tachycardia, with little effect on the pressor effects of central bradykinin (20 micrograms). The results indicate that centrally administered bradykinin stimulates vasopressin release into the plasma and that central vasopressin may modulate the cardiovascular actions of central bradykinin.

Animals↗
PubMed1986

Prevention of arginine-vasopressin-induced motor disturbances by a potent vasopressor antagonist.

The antivasopressor analog d(CH2)5Tyr(Me) arginine-vasopressin completely blocked the convulsive-like behavior and other severe motor disturbances which are normally observed following a second central arginine-vasopressin injection. This vasopressor antagonist appears to be selective for arginine-vasopressin-induced motor disturbances, in that the convulsive and motor effects of pentylenetetrazol and somatostatin were not altered significantly by pretreatment with the central antagonist. Results suggest that arginine-vasopressin-induced motor disturbances are mediated via central receptors. The classic antidiuretic (V2) type of arginine-vasopressin receptor does not appear to be involved, since the agonist 1-desamino-8-D-arginine-vasopressin did not elicit convulsive-like behavior or other severe motor disturbances 2 days following a first ('priming') injection of arginine-vasopressin.

Animals↗