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PubMed1988

Evidence of two steps in the homologous desensitization of vasopressin-sensitive phospholipase C in WRK1 cells. Uncoupling and loss of vasopressin receptors.

The exposure of WRK1 cells to arginine vasopressin (AVP), lysine vasopressin, or oxytocin for 18 h at 37 degrees C induced a homologous desensitization of the vasopressin- (VP) receptors. Dose-response curves of [3H]lysine vasopressin binding to control and desensitized WRK1 cells revealed a decrease in the maximal number of binding sites without any modification of its affinity (Kd values = 4.40 +/- 0.76 nM and 4.65 +/- 0.78 nM for control and desensitized conditions, respectively). The phenomenon was time- and dose-dependent. It was directly related to receptor occupancy, since the concentration of VP analogues leading to a half-maximal occupancy of VP receptors was closely related to the concentration of the corresponding analogue leading to a half-maximal decrease in VP-binding sites. It was also agonist-specific, since the V1 vasopressin antagonist desGly9d(CH2)5[D-Tyr(Et)2]VAVP was unable to affect the number of receptors. These desensitization processes were completely inhibited when the functional coated pits present in WRK1 cells were suppressed, indicating that the loss of VP-binding sites was related to receptor internalization. The exposure of WRK1 cells to a vasopressin agonist for 18 h also led to an inhibition of the vasopressin-sensitive phospholipase C activity. It was time- and agonist-dose-dependent, and occurred without any detectable changes in apparent affinity values (1.40 +/- 0.04 and 1.90 +/- 0.36 nM for control and desensitized cells, respectively). Control experiments showed that these inhibitions could not have been caused by a decrease in the labeling of inositol lipids. It is likely that they were mainly due to receptor internalization since (i) the hormonal treatment did not modify the basal level of phospholipase C; (ii) the maximal loss of VP-binding site was similar to the maximal inhibition of VP-stimulated IP accumulation; (iii) the recoveries of both VP-binding sites and VP-sensitive phospholipase C activity followed exactly the same time course (t1/2 = 4 h). In addition to this homologous desensitization of VP-sensitive phospholipase C activity, AVP also induced heterologous desensitization of bradykinin-sensitive phospholipase C activity. However, this effect was relatively weak (maximal inhibition 17 +/- 3%). The time course of VP-sensitive phospholipase C desensitization was more rapid than that of VP-receptors, indicating that desensitization involved at least two distinct steps, a rapid uncoupling step, and a later loss of vasopressin receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Vasopressin receptors in human pregnant myometrium and decidua: interactions with oxytocin and vasopressin agonists and antagonists.

Saturation analysis and competition experiments were performed to identify and characterize [3H]arginine vasopressin binding to human myometrium and decidua in late pregnancy. [3H]Arginine vasopressin bound with affinity similar to that of [3H]oxytocin to both tissues (dissociation constant 1 to 2 nmol/L). The concentration of [3H]arginine vasopressin binding sites was high, particularly in decidua, but in all instances was about 50% to 60% of [3H]oxytocin binding. Analogs with selective oxytocic potency (4-threonine oxytocin, isotocin) had high affinity to both [3H]arginine vasopressin and [3H]oxytocin binding sites, as did analogs with both oxytocic and vasopressor activity (vasotocin). Analogs with selective antidiuretic activity (1-deamino-8-D-arginine vasopressin) showed drastically reduced affinity to [3H]oxytocin binding sites and relatively low but significantly higher affinity to [3H]arginine vasopressin binding sites. A new oxytocin antagonist (RW22164 or [1-deamino-2D-tyrosine-(O-ethyl)-4-threonine-8-ornithine]oxytocin) competitively bound to both binding sites. Its affinity to [3H]oxytocin binding sites was greater than to [3H]arginine vasopressin binding sites whereas the relative affinities of a predominantly vasopressor antagonist [Manning compound) were reversed, suggesting the presence of distinct receptors for oxytocin and arginine vasopressin in pregnant human myometrium and decidua.

Animals↗
PubMed1989

The effects of infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin on common carotid vascular resistance in conscious, Long Evans rats.

1. Intravenous infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin (DDAVP) were given to conscious, Long Evans rats chronically instrumented with bilateral, common carotid, pulsed Doppler probes and intravascular catheters. 2. During infusion of vasopressin at 0.3 nmol min-1 there was an increase in common carotid vascular resistance with no change in mean blood pressure or heart rate. Following infusion there was a common carotid vasodilatation. 3. During infusion of vasopressin at 3.0 nmol min-1 there were increases in mean arterial blood pressure and in common carotid vascular resistances, accompanied by bilateral reductions in flow and in heart rate. Administration of (+)-(CH2)5Tyr(Et)DAVP (a V1-receptor antagonist), during the continued infusion of vasopressin, reversed the effects of the latter on mean blood pressure and heart rate; under these conditions there were increases in common carotid blood flows above baseline, in company with bilateral vasodilatations. The latter effects persisted after cessation of vasopressin infusion. 4. Infusions of DDAVP were without significant effects on any measured cardiovascular variable. 5. The results do not provide straightforward support for the claim that vasopressin acts to promote cerebral perfusion, at least when V1-receptor effects are unopposed. Furthermore, it seems likely tha the vasodilator influence of vasopressin on the common carotid vascular bed is not due to stimulation of V2-receptors.

Animals↗
PubMed2003

Vasopressin mediates neuroprotection in mice by stimulation of V1 vasopressin receptors: influence of PI-3 kinase and gap junction inhibitors.

Neuroprotective effect of vasopressin analogues, arginine Vasopressin (AVP) and lysine Vasopressin (LVP) was evaluated against MgCl2 induced cerebral ischemia model. AVP significantly prevented (P < 0.01) MgCl2 (1M) induced cerebral ischemia as compared to lysine Vasopressin (LVP) which was less effective (P < 0.05). Pretreatment with PI-3 kinase inhibitors, Wortmannin and LY-294002 (50 microg/kg, ip) significantly attenuated the protective effects of vasopressin. AVP was also effective in reducing the maximal electroshock (MES) induced convulsive time and this protective effect was blocked by PI-3 kinase inhibitors. On the other hand, pretreatment with gap junction intracellular communication (GJIC) blocker, mephenamic acid (30 mg/kg, ip) significantly potentiated the MgCl2 induced cerebral ischemia. This enhancement of cerebral ischemia was not reversed by vasopressin analogue, LVP. The role of V1 vasopressin receptor was evaluated by pretreating the animals with non-selective V1 receptor antagonist, des Gly-NH2, d (CH2)5 [D-Tyr2, Thr4] OVT which reversed the effects of AVP suggesting a role for vasopressin V1 receptors. This study suggests that neurohypophyseal hormone, AVP is neuroprotective against MgCl2 induced cerebral ischemia and this effect is modulated by PI-3 kinase enzyme inhibitors and protein kinase C inhibitors through possible influence on the cerebral vascular tone. This study suggests that gap junctions have potential role in the induction of MgCl2 induced cerebral ischemia.

Animals↗
PubMed1986

Effects of vasopressin and La3+ on plasma-membrane Ca2+ inflow and Ca2+ disposition in isolated hepatocytes. Evidence that vasopressin inhibits Ca2+ disposition.

Vasopressin caused a 40% inhibition of 45Ca uptake after the addition of 0.1 mM-45Ca2+ to Ca2+-deprived hepatocytes. At 1.3 mM-45Ca2+, vasopressin and ionophore A23187 each caused a 10% inhibition of 45Ca2+ uptake, whereas La3+ increased the rate of 45Ca2+ uptake by Ca2+-deprived cells. Under steady-state conditions at 1.3 mM extracellular Ca2+ (Ca2+o), vasopressin and La3+ each increased the rate of 45Ca2+ exchange. The concentrations of vasopressin that gave half-maximal stimulation of 45Ca2+ exchange and glycogen phosphorylase activity were similar. At 0.1 mM-Ca2+o, La3+ increased, but vasopressin did not alter, the rate of 45Ca2+ exchange. The results of experiments performed with EGTA or A23187 or by subcellular fractionation indicate that the Ca2+ taken up by hepatocytes in the presence of La3+ is located within the cell. The addition of 1.3 mM-Ca2+o to Ca2+-deprived cells caused increases of approx. 50% in the concentration of free Ca2+ in the cytoplasm [( Ca2+]i) and in glycogen phosphorylase activity. Much larger increases in these parameters were observed in the presence of vasopressin or ionophore A23187. In contrast with vasopressin, La3+ did not cause a detectable increase in glycogen phosphorylase activity or in [Ca2+]i. It is concluded that an increase in plasma membrane Ca2+ inflow does not by itself increase [Ca2+]i, and hence that the ability of vasopressin to maintain increased [Ca2+]i over a period of time is dependent on inhibition of the intracellular removal of Ca2+.

Animals↗
PubMed2003

Intermittent footshock facilitates dendritic vasopressin release but suppresses vasopressin synthesis within the rat supraoptic nucleus.

Emotional stress inhibits vasopressin release from the pituitary but may facilitate its release from the dendrites in the hypothalamus. We examined effects of intermittently applied footshock upon the amount of vasopressin heteronuclear RNA in the hypothalamus. The footshock decreased plasma vasopressin concentration but increased its extracellular concentration within the supraoptic nucleus. The contents of the vasopressin heteronuclear RNA in the supraoptic nucleus were significantly decreased after the shock. These data suggest that intermittent footshock decreases not only vasopressin release from the axon terminals in the pituitary, but also vasopressin synthesis in the cell bodies in the hypothalamus while the stimulus facilitates vasopressin release from the dendrites in the hypothalamus. The data also suggest differential control of dendritic vasopressin release and synthesis in the hypothalamus.

Animals↗
PubMed1986

Effect of haemorrhage on plasma lysine vasopressin and the cardiovascular responses to vasopressin in the pig fetus.

The effect of haemorrhage on plasma lysine vasopressin concentrations and the cardiovascular effects of intravenous injections of synthetic lysine vasopressin were studied in twenty-four chronically catheterized pig fetuses aged between 81 and 114 d gestation (term = 114 +/- 1 d). Removal of 15-20% of the estimated blood volume reduced mean arterial blood pressure and elevated plasma vasopressin concentrations above the mean basal value of 2.2 +/- 0.3 muu./ml. The vasopressin concentration in plasma of fetuses younger than 104 d was insignificantly affected at 30 and 60 min after the bleed, whereas the corresponding values in older fetuses were raised by 12.7 +/- 7.2 muu./ml (d.f. = 7) and 16.0 +/- 6.0 muu./ml (d.f. = 7) respectively. The pituitary concentration of vasopressin was also greater towards the end of gestation. Plasma osmolality was unaffected by fetal blood loss. Maternal concentrations of vasopressin did not change from the basal values of 1.0 +/- 0.1 muu./ml (d.f. = 16). Injection of vasopressin raised fetal blood pressure and decreased heart rate. These results demonstrate that lysine vasopressin is present in the circulation of the pig fetus at 81 d (0.72 gestation), and that near term fetuses respond to haemorrhage more rapidly, and to a greater degree than younger fetuses.

Animals↗
PubMed1982

Central infusion of vasopressin decreased plasma vasopressin concentration in dogs.

The effects of increasing the cerebrospinal fluid (CSF) vasopressin concentration (CSFADH) by intracerebroventricular infusion of vasopressin on the plasma vasopressin concentration (PADH) were studied in four groups of anesthetized dogs. One group received an intracerebroventricular infusion of artificial CSF (ACSF) alone for 90 min; the other groups were infused intracerebroventricularly with vasopressin at rates of 10, 20, or 50 microunits/min for 90 min. Arterial blood and CSF samples were taken just before infusion and at 30-min intervals for 210 min. Vasopressin infused intracerebroventricularly at 10, 20, and 50 microunits/min resulted in peak CSFADH of 32.2 +/- 5.3, 82.6 +/- 4.5, and 131.4 +/- 12.5 microunits/ml and reductions in PADH of 32, 47, and 51%, respectively. Only the latter two responses were significant (P less than 0.5-0.01). Because the peak increases in CSFADH after intracerebroventricular infusion of vasopressin ranged from values that were similar to or five times higher than those seen after severe hemorrhage or intracerebroventricular hypertonic saline infusion, we suggest that centrally acting vasopressin may play a physiological role in control of vasopressin secretion.

Animals↗
PubMed1981

Nature of the immunoreactive neurophysins in ectopic vasopressin-producing oat cell carcinomas of the lung. Demonstration of a putative common precursor to vasopressin and neurophysin.

In an attempt to delineate the nature of the immunoreactive neurophysins in oat cell carcinomas of the lung with ectopic vasopressin production, tumor neurophysins were characterized by gel filtration and by electrophoresis. In all of the five tumor tissues, activities of both vasopressin and nicotine-stimulated neurophysin (NSN) determined by radioimmunoassay were demonstrated. A small amount of oxytocin as well as estrogen-stimulated neurophysin was detected in three of the tissues. When tissue extract was subjected to Sephadex G-50 gel filtration in 0.2 N acetic acid, the major portion of immunoreactive NSN emerged in the fractions corresponding to the molecular size of 10,000. The migration pattern of NSN in these fractions on electrophoresis was qualitatively the same as that of NSN extracted from human posterior pituitary glands. In addition to this major neurophysin, immunoreactive NSN with the molecular size of 20,000 was consistently demonstrated in three tumor extracts. This high molecular weight form of neurophysin represented 6.5--8.7% of total NSN immunoactivities in each tumor extract and its elution profile was not changed when analyzed under denaturating conditions in 6 M guanidine hydrochloride. On electrophoresis, it migrated near the gamma globulin region; however, the peak was broad suggesting that it consists of more than two different molecular populations. A substantial portion of the high molecular weight NSN appears to be a glycoprotein judging from its binding to concanavalin A. When the high molecular weight from of neurophysin was incubated with trypsin, essentially all of the activities were converted into NSN with the molecular size of 10,000. Moreover, an equimolar amount of vasopressin was liberated after the treatment, the elution pattern of which closely resembled that of synthetic arginine vasopressin. When a lower concentration of trypsin was used, some of the 20,000-dalton neurophysin exhibited activities of both NSN and vasopressin. Since the antivasopressin serum used in this study appeared to be directed toward the ring portion side of vasopressin, these results suggest that this 20,000-dalton neurophysin is, in all probability, a common precursor to vasopressin and neurophysin, and that vasopressin may be located in the middle of the precursor molecule.

Aged↗
PubMed1997

1-desamino-8-D-arginine vasopressin (DDAVP) as an agonist on V1b vasopressin receptor.

1-desamino-8-D-arginine vasopressin (DDAVP) is considered a standard vasopressin V2 receptor-selective agonist with a potent antidiuretic effect through V2 receptor without the induction of vasoconstriction through V1a receptor. Furthermore, DDAVP was reported to act as an agonist on non-V1a, non-V2 receptor to cause the accumulation of intracellular Ca2+ in several tissues. However, the agonistic activity of DDAVP against the other vasopressin receptor, V1b (or V3), which can accumulate intracellular Ca2+ and which we recently cloned, has not been clarified. Hence, we compared the characteristics of DDAVP on V1b receptor with those on the other vasopressin receptors. In binding experiments, DDAVP more strongly inhibited [3H]arginine vasopressin binding to V1b than to V2 receptor (Ki: 5.84 nM vs 65.9 nM). In addition, DDAVP dose-dependently stimulated inositol turnover in human V1b receptor-expressing COS-1 cells. DDAVP acted as a full agonist on human V1b receptor (EC50: 11.4 nM) as well as on human V2 receptor (EC50: 23.9 nM). However, DDAVP behaved as a partial agonist toward rat V1b receptor (intrinsic activity: 0.7, EC50: 43.5 nM), while there was no significant difference in the agonistic properties of arginine vasopressin on human and rat V1b receptor. In conclusion, DDAVP acts as an agonist on V1b receptor, as it does on V2 receptor. These findings will allow us to better understand the physiological role of V1b receptor in pancreatic beta cells and in the renal inner medullary collecting duct, and help us to identify as yet unknown vasopressin receptors through which DDAVP cause the accumulation of intracellular Ca2+ in other tissues.

Animals↗
PubMed1994

The effects of subcutaneous administration of arginine-8-vasopressin on the electroencephalogram of conscious rats are mediated by peripheral vasopressin V1 receptors.

The effects of subcutaneous (s.c.) administration of arginine-8-vasopressin (AVP) were investigated on the electroencephalogram (EEG) of conscious rats. AVP (1 mcg/kg) had no effect on the EEG. However, AVP (5 and 10 mcg/kg) produced significant changes in the spectral power of the EEG in a manner that was consistent with increase in level of arousal. Analogs of AVP which are virtually devoid of vasopressin V1 receptor agonist activity, desglycinamide-9 arginine-8 vasopressin (10 mcg/kg, s.c.) and 1-deamino-8-D arginine-8 vasopressin (10 mcg/kg, s.c.), had no effect on the EEG. Pretreatment with 1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid)2(O-methyl)tyrosine arginine-8 vasopressin (10 mcg/kg), a vasopressin V1 receptor antagonist, abolished the effects of AVP (10 mcg/kg) on the EEG. As systemically administered AVP cannot cross the blood-brain barrier, the present results indicate that the effects of s.c. AVP on the EEG of conscious rats are mediated by peripheral vasopressin V1 receptors.

Animals↗
PubMed1990

Determination of a suitable dosage of lysine-vasopressin and triglycyl-lysine-vasopressin, given in a gel-solution locally in the rectum of rats for possible radioprotective purposes.

In order to develop a method for selective radioprotection of the rectal mucosa, a dose-response study was carried out using triglycyl-lysine-vasopressin and lysine-vasopressin. The vasopressin was dissolved in a gel-solution of either Blanose (sodium-carboxymethyl-cellulose), Klucel (hydroxypropyl-cellulose) or Natrosol (hydroxyethyl-cellulose). The solution had a higher viscosity than water thus enabling rectal administration of the drug without any operative measures. The maximum vasopressin dose that can be given without causing any significant changes in systemic circulation was determined for the different solutions and vasopressins. For triglycyl-lysine-vasopressin this dose was 1,600 micrograms when it was dissolved in Blanose and 128 micrograms when dissolved in Natrosol. Lysine-vasopressin could be given in a maximum dose of 16 micrograms dissolved in Natrosol. Klucel solution did not seem suitable for this purpose. For further investigations, 16 micrograms lysine-vasopressin dissolved in Natrosol seems to be the most promising combination.

Administration, Rectal↗
PubMedDate not supplied

Vasopressin receptor distribution in adrenalectomized rats using vasopressin anti-idiotype.

Following adrenalectomy, it has been demonstrated that parvocellular corticotropin-releasing factor-containing neurons in the paraventricular nucleus (PVN) of rat hypothalamus synthesize vasopressin. The present study examined whether putative vasopressin receptors are expressed in parallel with the appearance of vasopressin immunoreactivity in these parvocellular neurons. A vasopressin anti-idiotypic antibody which immunostains putative vasopressin receptors associated with magnocellular PVN neurons was utilized. Following adrenalectomy, antivasopressin immunostained neurons in parvocellular and magnocellular PVN, whereas the anti-idiotypic antibody immunostained magnocellular neurons only. We therefore conclude that the putative vasopressin receptor recognized by the anti-idiotype is not demonstrated in association with parvocellular vasopressin-producing neurons of the adrenalectomized rat.

Adrenalectomy↗
PubMed2002

Effectiveness of hormonal tourniquet by vasopressin during myomectomy through vasopressin V1a receptor ubiquitously expressed in myometrium.

To elucidate the mechanism by which myometrial vasopressin injection promotes hemostasis during myomectomy, we examined the expression of vasopressin V1a receptor transcripts in the myometrium. Vasopressin V1a receptor expression was ubiquitous, and the transcripts were detected in the myometrium not only of cycling and pregnant patients, but also of postmenopausal or GnRH agonist-treated patients. Based on these observations, we applied intraoperative myometrial vasopressin injection during myomectomy in a non-randomized study in a total of 84 patients. Vasopressin injection significantly reduced the intraoperative blood loss and postoperative hemoglobin fall in patients without and with GnRH agonist pretreatment. No serious complications occurred on account of the vasopressin injection. We conclude that intraoperative vasopressin injection is effective as a hormonal tourniquet even in GnRH agonist-pretreated myomectomy.

Adult↗