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PubMed1986

Hypothalamic knife cuts alter vasopressin induced recovery of blood pressure following hemorrhage.

Effects of knife cuts posterior to the paraventricular nucleus (PVN) alone or to both the PVN and the supraoptic nucleus (SON) on vasopressin dependent restoration and maintenance of blood pressure following hemorrhage were tested in the rat. Conscious, unrestrained animals were hemorrhaged a volume equivalent to 1.8% of body weight from a femoral arterial catheter. Blood pressure was monitored for 30 min with no treatment, 30 min following iv injection of a specific antagonist to the pressor action of vasopressin, and 15 min during iv infusion of the competitive blocker of angiotensin II, saralasin. Restoration of blood pressure and the decrease in blood pressure with vasopressin blockade in rats with knife cuts posterior to the PVN alone were similar to that of control-operated animals. However, if knife cuts extended to the level of the SON, blood pressure was not restored, and vasopressin blockade did not result in a reduction of blood pressure. Saralasin infusion produced a similar decrease in blood pressure in all groups of animals. These data show that when knife cuts are confined to the area posterior to the PVN, vasopressin contributes to the restoration of blood pressure following hemorrhage. However, when cuts extend into the ventral hypothalamus, the contribution of vasopressin is eliminated.

Adaptation, Physiological↗
PubMed1981

Plasma vasopressin during insulin withdrawal in insulin-dependent diabetes.

Plasma vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis. During the 24 h period of insulin withdrawal, blood glucose rose from 6.7 +/- 1.0 to 20.7 +/- 2.4 mmol/l, whereas plasma vasopressin was 3.6 +/- 0.5 pg/ml initially and in four patients showed little change. Markedly elevated levels of plasma vasopressin (17.8, 19.8 and 26.6 pg/ml) were observed in three patients following the onset of hypovolaemia, nausea and/or vomiting which are known to stimulate vasopressin release. Free water clearance was negative throughout the study in all patients. Thirst was not noted despite marked hyperglycaemia (16.9 +/- 2.5 mmol/l) until a significant fall in body weight of 0.9 +/- 0.2 kg had occurred (p less than 0.005). We concluded that marked elevation of vasopressin results from non-osmotic stimulation and that the mechanisms of body water conservation are overridden by the glycosuric diuresis.

Adult↗
PubMed1995

Oxytocin-producing and vasopressin-producing eosinophils in the mouse spleen: immunohistochemical, immuno-electron-microscopic and in situ hybridization studies.

Oxytocin-like and vasopressin-like immunoreactive cells, and the cells expressing mRNAs for these peptides in the spleen of the C57BL/6 mouse were studied by immunohistochemistry, immuno-electron microscopy and in situ hybridization. Immunoreactive cells were distributed mainly in the splenic cord and marginal zone, whereas there were few in the lymphocyte-packed periarteriolar-lymphoid sheath, lymphoid follicle and germinal center. More numerous vasopressin-positive cells were seen in the splenic cord. The colocalization of oxytocin-like and vasopressin-like immunoreactivity in the same cells was identified by the investigation of mirror sections. By the pre-embedding immuno-electron-microscopic method using antisera against oxytocin and vasopressin, immunopositive reaction products were localized in the matrix around the specific granules, small clear vesicles and mitochondrial membrane of the eosinophils. No immunoreactivity to these peptides was found within the specific granules of the eosinophils. In situ hybridization with synthetic oligonucleotide probes labeled with 32P revealed the presence of mRNAs for oxytocin and vasopressin in the cells of the spleen, the distribution of the mRNAs for these peptides being the same as that of immunopositive cells. These observations suggest that eosinophils synthesize both oxytocin and vasopressin and store them in the matrix. Possible differences in the mechanism of synthesis and storage of these peptides between peripheral eosinophils and hypothalamic neurons are discussed.

Animals↗
PubMed1990

Impaired hydroosmotic response to vasopressin of cortical collecting tubules from lithium-treated rabbits.

The hydroosmotic action of [arginine]vasopressin (vasopressin, 25 microU/ml) and of 8-Br-cAMP (10(-4)M) was studied in vitro in perfused cortical collecting tubules (CCT) isolated from rabbits fed with lithium chloride for 3 weeks. Vasopressin-dependent water reabsorption was significantly inhibited by 65% although no lithium was used in the in vitro experiments. The hydroosmotic action of 8-Br-cAMP was also inhibited by previous Li treatment, but the effect was smaller in magnitude. Water intake, diuresis, and urinary osmolality were no different in the lithium-treated animals as compared with respective pretreatment values or with control animals given an equivalent amount of sodium chloride. Neither the creatinine clearance nor the maximal urinary concentrating ability were modified by lithium treatment. A mathematical model simulating water reabsorption along the CCT predicts that a 65% reduction of vasopressin-stimulated hydraulic conductivity, as observed in the Li group, may not be sufficient to prevent a complete osmotic equilibration at the end of the CCT in vivo. We conclude that: (a) in the rabbit, lithium administration induces an impairment of the hydroosmotic action of vasopressin in the CCT, which is due to an inhibition of pre- and post-cAMP events. (b) The inhibition of vasopressin action can be demonstrated in vitro at a time when no detectable impairment of the water conservation process occurs in vivo.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1984

Immunocytochemical localization of peptidergic cells in the neuro-endocrine system of the Colorado potato beetle, Leptinotarsa decemlineata, with antisera against vasopressin, vasotocin and oxytocin.

Antisera against vasopressin, vasotocin, oxytocin, neurophysin-1 and neurophysin-2 were used to investigate immunocytochemically the presence of neurons containing substances antigenically related to these peptides in the nervous system of the Colorado potato beetle. Ten different antisera were used, four against vasopressin, three against oxytocin and one against vasotocin, neurophysin-1, and neurophysin-2. Immunoreactivity was shown by all antisera except those against the neurophysins. The vasopressin antisera all gave different results. One antiserum revealed only a single neuron pair, whereas others revealed in addition one or two other different cell groups. The oxytocin antisera likewise revealed different neurons. The fixation procedure influenced the outcome of the immunocytochemical reaction. Immunoreactivity as revealed by vasopressin, vasotocin and oxytocin antisera is often co-localized in the same neurons; solid phase adsorptions showed that this is due to cross-reactivity of the antisera. Some of the immunoreactive neurons are identical to those recently described to contain a bovine pancreatic polypeptide/FMRFamide-like peptide. This co-localization is probably not due to a cross-reaction. These findings indicate the presence of several vasopressin-like and oxytocin-like substances which in the Colorado potato beetle all have a different degree of immunocytochemical resemblance to vasopressin and oxytocin.

Animals↗
PubMed1992

Decrease in hypothalamic vasopressin mRNA poly(A) tail length following physiological stimulation.

1. The vasopressin mRNA in the adult male rat hypothalamus is modulated in two distinct ways by a dehydration stimulus. In addition to the well-established increase in transcript abundance, it has recently been demonstrated that the vasopressin mRNA poly(A) tail increases in length. 2. We have studied the ontogeny of poly(A) tail length modulation in neonates in response to milk deprivation and found that poly(A) tail length changes are age dependent. In neonates older than 12 days of age, the vasopressin mRNA poly(A) tail length increased with milk deprivation and this effect became more marked in older animals. However, in rats 5 to 9 days old, milk deprivation resulted in a detectable though not significant decrease in vasopressin mRNA poly(A) tail length. 3. As milk deprivation is a combination of dehydration and starvation, we investigated the effect of the latter stimulus in more mature animals. We found that starvation modifies the length of the vasopressin mRNA poly(A) tail in a manner opposite that due to dehydration. 4. Our data indicate a novel mode of regulation of the vasopressin mRNA, namely, poly(A) tail shortening. This system provides a model for future studies concerning the adaptive role of poly(A) tail length modulation in response to physiological stimuli.

Adaptation, Physiological↗
PubMedDate not supplied

Effects of arginine-vasopressin on regional blood volume distribution in supine humans.

In healthy humans, the increase in arterial blood pressure seen in patients with autonomic dysfunction in response to exogenous vasopressin (AVP) is abolished. We tested the hypothesis that redistribution of blood from the intra- to the extrathoracic vascular compartment might contribute to this buffer response. Regional distribution of 99mTc labeled autologous red cells was assessed in healthy supine volunteers (n = 7) during arginine-vasopressin administration (1 ng.kg-1 bolus i.v. followed by a 14-min infusion of 3 ng.kg-1 x min-1), along with arterial and central venous pressures, and heart rate. Exogenous vasopressin increased plasma vasopressin concentration from 4.0 +/- 1.4 SEM to 91 pg.ml-1 +/- 12. Thoracic counts increased slightly but significantly by 2.2% +/- 0.9, while global abdominal counts remained unchanged. Most surprisingly, counts in the liver markedly increased (+8.1% +/- 1.8, p = 0.02), but significantly decreased in the spleen (-3.1% +/- 1.4). Intestinal (-2.5% +/- 2.4) and limb counts did not change significantly. Consistent with the increase in thoracic counts central venous pressure increased from 3.6 mmHg +/- 1 to 4.7 +/- 1 (p = 0.02), while arterial pressure and heart rate did not change. All changes reversed towards baseline when vasopressin administration ceased. Thus, in humans with an intact autonomic system, vasopressin, at concentrations observed during hypotension, increases liver and, albeit to a small extent, also thoracic blood volume, but decreases splenic blood content. These results: 1) are incompatible with the hypothesis that AVP induces a shift of blood from intra- to extrathoracic capacitance vessels, and 2) show that AVP increases rather than decreases central blood volume.

Adult↗
PubMed1985

The effects of vasopressin on hepatic haemodynamics in the cirrhotic and non-cirrhotic rat.

Liver blood flow (xenon-133 clearance method) and portal venous flow were measured in cirrhotic and non cirrhotic rats following the infusion of vasopressin at varying rates. At low rates of infusion, vasopressin had no significant effect on portal venous flow or liver blood flow in cirrhotic or non-cirrhotic rats. Infusion of vasopressin at a rate of 0.08 microU/g body wt/min in non-cirrhotic rats and 0.04 and 0.08 microU/g body wt/min in cirrhotic rats decreased portal venous flow and increased liver blood flow. At higher rates of infusion (0.2 microU/g body wt/min in non-cirrhotic rats and 0.16 microU/g body wt/min in cirrhotic rats) these effects were reversed. Furthermore, an infusion of 0.08 microU/g body wt/min vasopressin significantly reduced portal pressure in the cirrhotic rat. However, portal pressure was not significantly altered following an infusion of 0.16 microU/g body wt vasopressin. The implications of these findings in relation to the possible deleterious effects of high rates of vasopressin infusion in the management of portal hypertension and bleeding oesophageal varices is discussed.

Animals↗
PubMed1985

Cerebrospinal fluid and plasma vasopressin during short-time induced intracranial hypertension.

The response of plasma and ventricular cerebrospinal fluid vasopressin concentration to short-time induced intracranial hypertension was studied in 8 patients with hydrocephalus, defined as ventricular enlargement on computerized tomography. In connection with measurement of conductance to cerebrospinal fluid outflow, the concentration of vasopressin in plasma and cerebrospinal fluid was measured during perfusion at a low (less than 10 mmHg) and at a high (greater than 20 mmHg) intraventricular pressure level. Mean plasma vasopressin concentration was increased from 2.4 +/- 0.4 pg/ml (SEM) during perfusion at the low pressure level to 4.2 +/- 0.8 pg/ml (p less than 0.01) at the high pressure level. The cerebrospinal fluid concentrations of vasopressin at the low and high intraventricular pressure were 1.2 +/- 0.1 pg/ml and 1.7 +/- 0.2 pg/ml (p less than 0.05), respectively. However, only half of the patients responded to the increase in intraventricular pressure with an increase in cerebrospinal fluid vasopressin concentration exceeding 50%. The results of the present study suggest that an increase in the intracranial pressure might be a stimulus for vasopressin release in both the blood and the cerebrospinal fluid.

Aged↗
PubMed1981

Structural responses to voltage-clamping in the toad urinary bladder. II. Granular cells and the natriferic action of vasopressin.

The natriferic action of vasopressin has been investigated with morphological studies of voltage-clamped toad urinary bladders. Granular cell swelling can be induced in the presence of isoosmotic solutions when the orientation of the transmural potential is reversed by voltage clamping (V.A. Bobrycki, J. W. Mills, A.D.C. Macknight & D. R. DiBona, J. Membrane Biol., 60:21, 1981) and results from an increased rate of sodium entry across the mucosal membrane; under these conditions the active transport mechanism at the basal-lateral membrane becomes rate-limiting. Vasopressin exacerbated the voltage-reversal-induced swelling of granular cells while other cell types were unaffected. Granular cell swelling appeared to be dependent upon sodium entry from the mucosal medium since it was completely prevented by amiloride. There was no evidence for an effect of vasopressin on tight junction permeability; voltage-reversal induced the same amount of junction blistering whether or not vasopressin was present. It is concluded that the predominant effect of vasopressin on transepithelial sodium transport is to increase the sodium conductance of the mucosal plasma membrane. As is the case with the hydroosmotic effect of the hormone, the natriferic action of vasopressin seems to be exerted primarily, if not entirely, on the granular cells.

Amiloride↗
PubMed1986

High potassium intake increases the plasma concentration and urinary excretion of vasopressin in the rat.

The effect of alterations of dietary potassium intake on the plasma concentration and the urinary excretion of vasopressin was studied in male rats. Ingestion of a high potassium diet resulted in increases in the plasma concentrations of potassium and vasopressin, systolic blood pressure, urine flow, and urinary vasopressin excretion. Ingestion of a low potassium diet had little effect on the plasma vasopressin concentration and systolic blood pressure but caused decreases in the plasma potassium concentration and urinary vasopressin excretion. The results indicate that physiological changes in the plasma potassium concentration or some other consequence of altered dietary potassium intake can affect vasopressin release and excretion.

Animals↗
PubMedDate not supplied

The effects of vasopressin on memory processes in Java monkeys.

The roles of vasopressin (arginine-vasopressin) in controlling conditioned operant food-procuring reflexes and various types of memory were studied in monkeys. Types of memory were: conditioned reflex, image (Hunter-Kerr test), short-term, and long-term. The effects of vasopressin were assessed in terms of objective measures of higher nervous activity: movement and autonomous functions. These studies showed that administration of vasopressin to monkeys had different effects on simple operant food-procuring responses and memory processes. Vasopressin had greater effects on memory processes and the restoration of memory after functional derangements of higher nervous activity. The question of the formation of the two types of effect of vasopressin on higher nervous activity is discussed in relation to the evolution of mammals.

Animals↗
PubMed2006

Vasopressin antagonists.

Effects of vasopressin via V1a- and V2-receptors are closely implicated in a variety of water-retaining diseases and cardiovascular diseases, including heart failure, hyponatraemia, hypertension, renal diseases, syndrome of inappropriate antidiuretic hormone secretion, cirrhosis and ocular hypertension. As vasopressin receptors are found in many different tissues, vasopressin antagonists may benefit the treatment of disorders such as cerebral ischaemia and stroke, Raynaud's disease, dysmenorrhoea and tocolytic treatment. V1b selective vasopressin antagonists are discussed in terms of their usefulness in the treatment of emotional and psychiatric disorders. The vaptans are vasopressin receptor antagonists with V1a (relcovaptan) or V2 (tolvaptan, lixivaptan) selectivity or non-selective activity (conivaptan) which may be advantageous in some disorders. The V1a/V2 non-selective vasopressin antagonist conivaptan is the first vaptan which is approved by the FDA for the treatment of euvolaemic hyponatraemia.

Animals↗
PubMed1992

Vasopressin stimulation of vanadate-sensitive Na+ transport by liver plasma membrane vesicles. Evidence for regulation via phospholipase C and protein kinase C activities.

The rate of vanadate-sensitive 22Na+ uptake by isolated liver membrane vesicles, reflecting transport by Na+/K(+)-ATPase, was measured to study the role played by phospholipase C and protein kinase C in the regulation of this process by vasopressin. Na+ uptake was enhanced 2-3-fold by 100 nM [Arg8]vasopressin and the hormone effect was mimicked by 0.1 microM inositol 1,4,5-trisphosphate as well as by 1.0 microM myo-inositol. The stimulation by vasopressin was potentiated by phosphatidylinositol-specific phospholipase C from Bacillus thuringiensis (5-10 mU/ml). No effect of the bacterial enzyme was observed in the absence of the hormone. Phorbol myristate acetate (0.5-1 microM) suppressed the stimulation by vasopressin but had no effect in the absence of the hormone. High concentrations of bacterial phosphatidylinositol-specific phospholipase C (50-100 mU/ml) also antagonized the hormone stimulation. Staurosporine (50-100 nM) prevented the antagonistic effect of bacterial phospholipase C (50 mU/ml) and EGTA (1 mM) partially protected the hormonal stimulation in the presence of phorbol myristate acetate. Our results suggest that the stimulatory effect of vasopressin on Na+ transport is mediated by phospholipase C and products derived from the inositol moiety of membrane phospholipids. Membrane-associated protein kinase C appears to be at least partially responsible for the desensitization to stimulation by vasopressin.

Animals↗
PubMed1987

Effects of vasopressin on the synthesis of phosphatidylethanolamines and phosphatidylcholines by isolated rat hepatocytes.

The effect of vasopressin on the biosynthesis of phosphatidylcholines and phosphatidylethanolamines was investigated in freshly isolated rat hepatocytes in suspension. Treatment of hepatocytes with vasopressin inhibits the incorporation of [Me-14C]choline into phosphatidylcholines in a dose-dependent manner. The hormone does not affect the uptake, phosphorylation or oxidation of choline. Pulse-chase studies indicate that CTP:cholinephosphate cytidylyltransferase might be subject to hormonal regulation by vasopressin. In contrast with the inhibitory effect of vasopressin on the synthesis of phosphatidylcholines, this hormone stimulates the incorporation of [1,2-14C]ethanolamine into phosphatidylethanolamines in a dose-dependent manner. Pulse and pulse-chase studies with labelled ethanolamine show that the conversion of ethanolaminephosphate to CDPethanolamine as well as the formation of phosphatidylethanolamines from CDPethanolamine and diacylglycerol are enhanced. Determination of the effect of vasopressin on the activity of the enzymes of the synthesis de novo of phosphatidylethanolamines demonstrates an increase of the activity of ethanolaminephosphotransferase, probably as a result of the increased amount of diacylglycerol in vasopressin-treated cells.

Animals↗
PubMed1990

Vasopressin and norepinephrine stimulation of inositol phosphate accumulation in rat hepatocytes are modified differently by protein f1nase C and protein kinase A.

Rat hepatocytes were maintained in primary monolayer culture for 24 h in the presence of serum. Treatment of hepatocytes with 1 microM 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) for 5-15 min increased membrane-associated protein kinase C activity and concomitantly decreased soluble activity. Membrane protein kinase C activity returned to basal values within 1 h then decreased by more than 50% within 2 h. Prolonged (2-18 h) incubation with PMA did not further decrease protein kinase C activity. Pretreatment of hepatocytes with PMA for 5-15 min had little effect on the subsequent actions of 100 nM vasopressin but abolished the stimulation of inositol phosphate accumulation by 3 nM vasopressin and 20 microM norepinephrine. Long-term exposure (2-18 h) of hepatocytes to 1 microM PMA actually enhanced the effects of vasopressin and 20 microM norepinephrine. The stimulation by norepinephrine (20 microM) of inositol phosphate accumulation was abolished by the alpha 1-adrenergic antagonist prazosin (1 microM), whereas the beta-adrenergic antagonist propranolol (30 microM) had little effect. Addition of 8Br-cAMP (100 microM) or glucagon (10 nM) for 5 min or 8 h had no significant effect alone, but enhanced the subsequent vasopressin stimulation of inositol phosphate accumulation. There was no effect of 8Br-cAMP or glucagon on norepinephrine stimulation of phosphoinositide breakdown. These data indicate that the stimulation of phospholipase C activity in rat hepatocytes by 3 nM vasopressin is enhanced by cyclic AMP-dependent kinase but inhibited by protein kinase C. In contrast, down regulation of protein kinase C markedly enhanced the maximal phosphoinositide response due to both vasopressin and norepinephrine.

Animals↗
PubMed1991

Effects of interleukins on plasma arginine vasopressin and oxytocin levels in conscious, freely moving rats.

To elucidate whether interleukins are involved in vasopressin or oxytocin release during cytokine-related stressful conditions, we examined the effects of human interleukin-1 beta and interleukin-6 on plasma vasopressin and oxytocin levels in rats. Interleukin-1 beta administrated intravenously stimulated both the vasopressin and oxytocin secretion in dose-dependent manners. Neither hormone release was observed following interleukin-6 administration. Pretreatment with aspirin significantly attenuated the effects of interleukin-1 beta on both the vasopressin and oxytocin levels. SC-19220, a prostaglandin E2 receptor antagonist, did not affect the interleukin-1 beta-induced increase of plasma oxytocin levels, but almost completely abolished its effect on plasma vasopressin levels. These results suggest that under certain stressful conditions which accompany the stimulation of cytokine production, interleukin-1 is involved in the increase of plasma vasopressin and oxytocin levels and, moreover, different kinds of prostaglandins are suggested to participate in these interleukin-1-induced hormone release.

Animals↗
PubMed1982

Increased formation of phosphatidic acid induced with vasopressin or Ca2+ ionophore A23187 in rat hepatocytes.

The effects of vasopressin and Ca2+ ionophore A23187 on phospholipid metabolism were investigated in rat hepatocytes. Vasopressin stimulated the incorporation of [32P]Pi into phosphatidic acid within 2 min but then it returned to control level after 10 min. On the other hand, the stimulation of the incorporation of [32P]Pi into phosphatidylinositol continued with incubation times up to 20 min. The Ca2+ ionophore A23187 also increased the 32P-labeling in phosphatidic acid, although it had no effect on [32P]Pi incorporation into phosphatidylinositol. Concerning the incorporation of [3H]glycerol, vasopressin did not enhance its incorporation into phosphatidic acid and phosphatidylinositol. The Ca2+ ionophore A23187 increased the incorporation into phosphatidic acid without significant effects on that into phosphatidylinositol. In the hepatocytes prelabeled with [3H]arachidonic acid, stimulated degradation of phosphatidylinositol with the addition of vasopressin and resultant formation of phosphatidic acid were observed within 5 min. The transient accumulation of diacylglycerol, the product of phosphatidylinositol hydrolysis, also occurred within 5 min with vasopressin. On the other hand, with the Ca2+ inophore A23187, stimulated degradation of triacylglycerol to diacylglycerol and the consequent formation of phosphatidic acid were observed. The Ca2+ ionophore A23187 caused a significant release of free [3H]arachidonic acid, although vasopressin had no effect.

Animals↗