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PubMed1989

The effects of vasopressin and related peptides on osmoregulation in Amoeba proteus.

We describe the effects of arginine-vasopressin (AVP) and five related peptides on the contractile vacuole, the osmoregulatory organelle of the fresh water Amoeba proteus. Arginine-vasopressin, lysine-vasopressin, and SKF 101926, a synthetic antagonist of vasopressin, cause a significant increase in the rate of output of the contractile vacuole. Deamino-vasopressin (dAVP), oxytocin, and arginine-vasotocin have no such activity, although dAVP interferes with the action of AVP when present in equimolar concentration. Relatively high concentrations are required and the effect of active peptides is readily reversible. When the normal, hypotonic medium (a synthetic pond water) is replaced by isotonic sucrose, the action of AVP on the vacuole is abolished. Thus vasopressin is believed to act by increasing permeability of the Amoeba plasma membrane to water.

Amoeba↗
PubMed1984

Interactions between CRF, epinephrine, vasopressin and glucocorticoids in the control of ACTH secretion.

The secretion of ACTH by corticotrophs in the anterior lobe of the rat pituitary gland is under the stimulatory influence of at least three receptors, namely that for peptidic CRF (corticotropin-releasing factor), vasopressin and alpha 1-adrenergic agents. CRF is a potent stimulator of cyclic AMP accumulation as well as adenylate cyclase activity in the rat adenohypophysis, thus suggesting an important role of cyclic AMP as mediator of CRF action on ACTH secretion. Vasopressin causes a 2-fold increase of the stimulatory effect of CRF on ACTH release in rat anterior pituitary cells in culture. The potentiating effects of vasopressin on CRF-induced ACTH release are accompanied by parallel changes of intracellular cyclic AMP levels. Vasopressin, while having no effect on basal cyclic AMP levels, causes a 2-fold increase in CRF-induced cyclic AMP accumulation without affecting the ED50 value of CRF action. ACTH secretion is also stimulated by a typical alpha 1-adrenergic receptor. Epinephrine causes a marked stimulation of ACTH release which is additive to that of CRF. Epinephrine, in analogy with vasopressin, although having no effect alone on basal cyclic AMP levels, causes a marked potentiation of CRF-induced cyclic AMP accumulation. Glucocorticoids cause a near-complete inhibition of epinephrine-induced ACTH secretion within 4 h with the following order of ED50 values: triamcinolone acetonide (0.2 nM) greater than dexamethasone (1.0 nM) much greater than cortisol (11 nM) greater than corticosterone (22 nM). Similar effects are observed for CRF- and vasopressin-induced ACTH release. Although the activity of the pituitary-adrenocortical axis in the rat is highly dependent upon sex steroids, 17 beta-estradiol, 5 alpha-dihydrotestosterone and the pure progestin R5020 have no detectable effect on basal or epinephrine-induced ACTH release, thus illustrating the high degree of specificity of glucocorticoids in their feedback control of ACTH secretion. Moreover, glucocorticoids have no effect on CRF-induced cyclic AMP accumulation, thus indicating that their inhibitory effect is exerted at a step following cyclic AMP accumulation.

Adenylyl Cyclases↗
PubMed1985

The effects of vasopressin and catecholamines on cyclic AMP in homogenates of rat brain.

Vasopressin is known to mediate its action on the kidney through increasing the concentrations of cyclic AMP. As vasopressin is widely distributed in many extra hypothalamic areas of the brain and can be shown to act centrally, we have investigated the effect of vasopressin on cyclic AMP levels in homogenates of the striatal and locus coeruleus areas. In contrast with the effect obtained on the kidney, vasopressin did not stimulate adenyl cyclase activity in rat brain homogenates in a dose-related manner. The stimulation of cyclic AMP observed with dopamine or noradrenaline in these brain areas and the hippocampus was not affected by the presence of vasopressin. These observations suggest that the action of vasopressin on the brain is not mediated through cyclic AMP.

Adenylyl Cyclases↗
PubMed1987

Trauma induced increases in plasma vasopressin and angiotensin II.

Previous investigators have shown that hypotension will cause an increase in plasma levels of both vasopressin and angiotensin II. Significant increases in peripheral resistance after thermal trauma suggested that a similar increase in plasma vasopressin and angiotensin II levels might occur under this condition. This possibility has been studied in the pentobarbital anesthetized dog. Peripheral resistance was calculated from measured cardiac output and mean arterial blood pressure. Vasopressin and angiotensin II levels were measured by radio-immunoassay. The results of this study showed that vasopressin plasma levels increase 4 to 6 fold 15 minutes after thermal trauma and remained elevated (3 to 4 fold) for at least 6 hours. Angiotensin II increased in a linear manner from 15 minutes to 6 hours post trauma. At 6 hours post trauma angiotensin II plasma levels were 4 times pretrauma levels. For the first 4 hours post trauma there was a positive correlation between the sum of vasopressin and angiotensin II plasma levels and the increase in peripheral resistance. These results suggest that the trauma induced increase in peripheral resistance is due to increases in plasma vasopressin and angiotensin II.

Angiotensin II↗
PubMed1981

Chlorpropamide effect: measurement of neurophysin and vasopressin in humans and rats.

The effect of chlorpropamide on neurohypophyseal function was studied by measurement of neurophysin and vasopressin in humans and in rats. Administration of chlorpropamide was shown to inhibit the ability of the human subjects and of the rats to maximally dilute their urine after administration of water. Comparison of the levels of vasopressin and neurophysin before and after the administration of chlorpropamide in the basal state and after water loading in both the human subjects and in rats showed no lack of suppression due to the chlorpropamide. The levels of both peptides were measured at the limits of detection. In other studies where neurophysin and vasopressin were readily detected, administration of chlorpropamide did not result in any augmented release of neurophysin or vasopressin in response to stimulation of the neurohypophysis in humans nor in rats. Levels of neurophysin in the pituitaries of rats showed no change in rats given chlorpropamide, while the content of vasopressin was increased, possibly indicating a chronic decreased secretion of vasopressin in rats given chlorpropamide.

Adult↗
PubMed1996

A randomized comparison of vasopressin and tourniquet as hemostatic agents during myomectomy.

OBJECTIVE: To assess the comparative efficacy of perivascular vasopressin and tourniquet in minimizing bleeding and its sequelae at myomectomy. METHODS: Between March 1994 and February 1995, 52 women with symptomatic uterine leiomyomas scheduled for myomectomy were entered into a randomized trial comparing vasopressin (26 patients) and tourniquet (26 patients) for hemostasis. Myomectomy was performed after either the perivascular injection of 20 U of vasopressin diluted to 20 mL with normal saline or with the use of a Foley catheter tourniquet around both uterine vessels. The efficacy of each method was measured by comparing differences in pre- and postoperative hemoglobin levels, intraoperative blood pressure, measured blood loss, need for blood transfusion, evidence of postoperative febrile morbidity, complications, and length of hospital stay. RESULTS: Vasopressin resulted in less blood loss (mean 287.3 mL [standard deviation (SD) 195] versus 512.7 mL [SD 400] for tourniquet [P = .036]). Six of 26 patients in the tourniquet group lost more than 1000 mL of blood, whereas all of the vasopressin subjects lost less than this amount (P = .023). However, there were no significant differences between the two groups in the fall in the hemoglobin level, number of blood transfusions given, intraoperative blood pressure, highest postoperative pulse and temperature, or other complications. CONCLUSION: Vasopressin prevents blood loss better than using the tourniquet during myomectomy.

Adult↗
PubMed1986

Endogenous vasopressin and the weaning period in Brattleboro rats.

Vasopressin, which is important for behavior and brain development, begins to influence osmoregulation with the onset of weaning. We studied the role of vasopressin in the development of feeding behavior since its mechanisms might be essential for the age determination of the suckling and weaning periods. Radionuclide methods were employed to follow maternal milk, solid food and water consumption in developing Brattleboro rats. The appearance of solid food intake and the spontaneous extinction of maternal milk intake indicated the onset and the end of weaning. The absence of endogenous vasopressin did not influence the onset and/or the duration of the weaning period. Both vasopressin-deficient homozygous Brattleboro rats and their heterozygous littermates (with preserved vasopressin synthesis) began to consume solid food and water at the age of 16 days and their intake of maternal milk was terminated about the 27th day of age. Thus, the maturation of feeding behavior in the suckling and weaning periods is vasopressin-independent.

Animals↗
PubMed1993

Effects of dehydration and rehydration on plasma vasopressin and aldosterone in horses.

We have investigated the change in plasma vasopressin and aldosterone concentrations in Namib (desert-adapted) and in control horses from a subtropical region, during an acute 12% dehydration and during rehydration, while food was available. During dehydration, vasopressin concentrations increased significantly in both groups of horses, but the increase was significantly greater in Namib horses than in control horses. During rehydration, vasopressin levels fell, but fell significantly less in Namib horses. The change in vasopressin concentration correlated significantly with plasma osmolality (r = 0.88, p < 0.001), and the relationship between these two variables was the same for both groups of horses during the dehydrated and rehydrated states. Aldosterone concentrations fell up to 48-h dehydration in both groups, but decreased significantly more in desert horses. From 48-h dehydration and during rehydration, aldosterone concentrations increased and the increase was sustained longer in Namib than in control horses. Changes in plasma osmolality did not correlate significantly with changes in aldosterone concentration. There were significant correlations between faecal moisture (%) and both vasopressin and aldosterone concentrations (r = -0.72, p < 0.008; r = 0.80, p < 0.002, respectively). During the 12% dehydration, the Namib horses sustained higher plasma osmolalities and consequently vasopressin levels than the control horses. We conclude that plasma osmolality in conjunction with these two hormones plays a significant role in water homeostasis in horses.

Acclimatization↗
PubMed1983

Vasopressin stimulates thromboxane synthesis in isolated hamster hepatocytes: relation to hepatocyte calcium content.

This study was designed to determine if vasopressin stimulates the formation of thromboxane B2 in freshly isolated hamster hepatocytes and if so, whether this thromboxane synthesis plays a role in the vasopressin-induced efflux of 45Ca++ from these cells. Thromboxane synthesis was found to be linear for 15 minutes, to be stimulated by arachidonic acid, and to be inhibited by indomethacin and by 7-(1-imidazolyl) heptanoic acid (7IHA), a selective inhibitor of thromboxane synthetase. Vasopressin stimulation of thromboxane synthesis was dose-related. Pretreatment with 7IHA and meclofenamate significantly increased basal 45Ca++ uptake by the cells. Neither 7IHA nor meclofenamate inhibited the ability of vasopressin to reduce the 45Ca++ content of the isolated hepatocytes. These results indicate that vasopressin stimulates thromboxane synthesis in hepatocytes but suggest that thromboxane does not play a role in the vasopressin-induced reduction in 45Ca++ content in this cell type.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Neurohypophysial peptides and the hippocampus. I. Vasopressin immunoreactivity in the rat hippocampus.

Immunocytochemical studies have demonstrated that nerve fibres containing immunoreactive vasopressin project to many areas of the central nervous system. In the present investigation, the presence of immunoreactive arginine vasopressin (IR-AVP) in the hippocampus of Wistar rats was confirmed by radioimmunoassay. The vasopressin content of the dorsal hippocampus was 30.3 +/- 7.3 pg IR-AVP/mg soluble protein (mean +/- SEM, n = 9) and that of the ventral hippocampus was 81.4 +/- 8.3 pg IR-AVP/mg soluble protein (n = 9), while tissue from the cerebral cortex contained no detectable vasopressin. That the immunoreactivity was due to vasopressin was confirmed by its absence in hippocampal or cortical tissue from homozygous Brattleboro rats, which are genetically unable to synthesize vasopressin.

Animals↗
PubMedDate not supplied

Sex-specific effects of met-enkephalin treatment on vasopressin immunoreactivity in the rat supraoptic nucleus.

The supraoptic nucleus of male and female rats treated with met-enkephalin or naloxone and met-enkephalin was examined with light microscopical immunocytochemistry for Arginine-vasopressin. Both genders exhibited the same distribution of immunostained magnocellular neurons. Met-enkephalin treatment caused an increase in number of immunostained vasopressin neurons. This effect was more pronounced in females than in males. Naloxone treatment diminished immunoreactive cytoplasmic vasopressin in males more effectively than in females. In enkephalin-treated animals numerous vasopressin immunoreactive varicosities appeared within the supraoptic nucleus, but were mostly absent in naloxone-treated animals and in controls. Our results indicate that met-enkephalin treatment either stimulates vasopressin synthesis or inhibits secretion. It is likely that steroid hormones mediate the action of enkephalin on vasopressin secretion in a specific manner.

Animals↗
PubMed1981

The effect of vasopressin in water-loaded hypokalemic patients is prostaglandin-independent.

Potassium-depleted subjects regularly excrete dilute urine with a high free-water clearance which cannot be suppressed either by solute loading or by water deprivation. In man, as in the dog and rat, potassium depletion impairs the ability of the kidney to achieve maximal urinary solute concentration and vasopressin is unsuccessful in overcoming this defect. In man and in the dog, potassium depletion induces a rise in urinary prostaglandin E2, an effect which can be reversed with indomethacin, a cyclo-oxygenase inhibitor. To evaluate the role of prostaglandins on the renal action of vasopressin in hypokalemia, six subjects with hypokalemia of various etiologies were studied in a control, drug-free condition and again after 3 to 6 days of indomethacin (100 mg/day). Renal clearance studies to measure the maximal free-water excretion in response to an intravenous water load (10 ml/min) and to a superimposed infusion of arginine vasopressin (40 mU/hr) were performed. The results in six patients are as follows: maximal free-water clearance (control) 8.03 +/- 0.8 ml/min (mean +/- S.E.), with the addition of vasopressin, .14 +/- 0.8; after 3 to 6 days of indomethacin, 8.55 +/- 1.33; with vasopressin 0.91 +/- 1.23 ml/min. There was no statistically significant difference between the maximal free water clearance with or without indomethacin. Vasopressin exerted an equally great response in both conditions and prostaglandins did not appear to play a role in free-water formation.

Adult↗
PubMed1993

Mapping of [3H]vasopressin binding sites in the brain of jerboa (Jaculus orientalis) by an high resolution beta-radio imager.

The distribution of vasopressin receptors in the brain of the jerboa (Jaculus orientalis) was studied using tritiated arginin vasopressin ([3H]vasopressin). beta-Particles emitted from tritiated ligand bound to brain sections were detected by a newly developed beta-radio imager to generate a light spot which was read by a charge coupled device camera. The number and coordinate of the center of gravity of the light spot were recorded. After summation in pixels of the counts collected during 2-20 h, an image was produced representing the distribution of [3H]vasopressin bound to brain sections. Specific vasopressin binding was detected in various brain regions such as the cerebral cortex, islands of Calleja, pallidum, amygdala and the hippocampus as well as in the pituitary gland. The intensity of the binding was quantified directly from the images obtained and expressed in decays/min/surface unit. The linearity of this method of detection allowed a relevant measurement of non-specific binding, therefore its subtraction from images representing the total binding. Three-dimensional reconstructions of labeled structures were also performed. The presence of numerous vasopressin receptors in the jerboa hippocampus suggests a major role for this neuropeptide in this part of the brain.

Animals↗
PubMed1994

Effects of vasopressin on regional cerebral blood flow in dogs.

Vasopressin may regulate the regional cerebral blood flow (rCBF) via two balancing effects: increased flow from the vessels dilated by nitric oxide from the endothelium, and decreased flow from the vessels contracted by direct stimulation of smooth muscle. The effect on the rCBF in anesthetized dogs following the intracisternal or intraarterial administration of vasopressin was investigated by laser flowmetry with the device placed on the dura over the parietal cortex. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF to 145.3 +/- 27.3% of base line. In contrast, the intravertebral arterial injection of vasopressin had no significant effect on the rCBF. This can be explained by a difference in the affected vasculature; mainly large vessels in the subarachnoid space vs. whole vascular system supplied by the vertebral artery. The intracisternal injection of 10 mumol of NG-monomethyl-L-arginine (L-NMMA) reduced the rCBF; pretreatment with this agent significantly suppressed the elevation in rCBF induced by vasopressin. The intraarterial injection of L-NMMA reduced the rCBF more than its intracisternal administration. It also suppressed the rCBF induced by vasopressin.

Animals↗
PubMed1986

Vasopressin and oxytocin in the developing rat brain as shown by isoelectric focusing of radioimmunoassayable peptides.

Vasopressin and oxytocin content were measured by radioimmunoassay in tissue extracts from rat pituitary, hypothalamus and the extrahypothalamic brain from gestational day 14 until postnatal day 14. Assayable compounds were subsequently characterized by isoelectric focusing in gels. Fetal day 14 extracts contained only low amounts of both hormones (around 1-2 pg per fetus). Vasopressin content rapidly increased to levels of 41 ng in pituitary, 20 ng in hypothalamus, 0.3 ng in extrahypothalamic brain on postnatal day 14. Oxytocin content showed only measurable amounts around day 20 prenatally, reaching levels of, respectively, 10, 0.5 and 0.2 ng on postnatal day 14. The presence of radioimmunoassayable vasopressin in the extrahypothalamic brain on fetal day 14 (around 2 pg) confirms the early ontogeny of vasopressinergic innervation of the brain. Whenever measurable, immunoreactivity had an isoelectric point similar to that of synthetic vasopressin or oxytocin. The possibility that the detected amounts of vasopressin were due to vasotocin, which had been claimed to be present in fetal brain, was excluded by comparison of the regression coefficients of serial dilutions of the extracts in the radioimmunoassay with those of synthetic vasotocin or vasopressin.

Animals↗
PubMedDate not supplied

Peripheral injections of vasopressin control behavior by way of interoceptive signals for hypertension.

The stimulus properties of peripheral injections of vasopressin were assessed using conditioned taste aversion techniques. Conditioned taste aversion induced by vasopressin was blocked by prior exposure to vasopressin but not to another aversive agent, apomorphine. Prior exposure to behaviorally equivalent doses of another hypertensive agent, angiotensin II, blocked also conditioned taste aversion induced by vasopressin and this effect was fully reciprocal, since prior exposure to AVP blocked the aversive effect of angiotensin II. The protection offered by prior exposure to angiotensin II was not due to an endogenous release of AVP since the aversive properties of angiotensin II were not blocked by administration of a specific antagonist of the vasopressor effects of vasopressin. These data suggest that the interoceptive cues which are responsible for the conditioned taste aversion induced by vasopressin are related to the hypertensive action of this peptide.

Angiotensin II↗
PubMed1987

Vasopressin does not hydrolyze polyphosphoinositides in rabbit papillary collecting tubule cells.

Changes in phosphatidylinositol metabolism are suggested to be involved in the mechanism of action of many membrane active hormones. We studied the effect of vasopressin on polyphosphoinositide metabolism in rabbit papillary collecting tubule cells to assess if the hydrolysis of these phospholipids is involved in transmembrane signaling. Rabbit papillary collecting tubule cells grown in monolayers for 5 days were labeled to constant specific activity with [3H]inositol. The temporal changes in [3H]inositol-labeled phospholipids were assessed in response to vasopressin. Similarly, water-soluble inositides were monitored after separation by ion exchange chromatography. Intracellular Ca2+ was monitored by use of the fluorescent indicator dye, quin2. Vasopressin (10(-7) M) did not increase the hydrolysis of phosphoinositides over a 5 min period when compared with controls. Similarly, there was no increase in water-soluble phosphoinositols during the same interval. Pretreating the cells with LiCl (10 mM) did not produce any increase in inositol 1-phosphate when stimulated with vasopressin but did in response to bradykinin. Finally, vasopressin did not increase cytosolic Ca2+ and did not increase the release of prostaglandin E2 into the media under our experimental conditions. We conclude that vasopressin does not stimulate prostaglandin E2 in rabbit papillary collecting tubule cells, does not initiate hydrolysis of polyphosphoinositides and does not increase cytosolic Ca2+. Thus these cells lack V1 receptor coupling mechanisms.

Aminoquinolines↗
PubMed1988

On the source of the vasopressin-induced increases in diacylglycerol in hepatocytes.

In hepatocytes pre-labelled with [3H]glycerol, vasopressin increased by 20% the amount of radioactivity present in diacylglycerols. The effect of vasopressin was partially dependent on Ca2+. The magnitude of the increase in [3H]diacylglycerol was 5-times the sum of the radioactivity present in phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate. No stimulation by vasopressin of the initial rate of incorporation of radioactivity into diacylglycerols was observed in cells incubated in the presence of 10 mM [3H]glycerol. Treatment of hepatocytes labelled with either [3H]ethanolamine or [3H]choline with vasopressin, ionophore A23187 or phospholipase C increased the amount of radioactivity present in trichloroacetic acid extracts of the cells. The effect of vasopressin was dependent on extracellular Ca2+. It is concluded that in hepatocytes vasopressin increases diacylglycerols by a process which does not principally involve the conversion of phosphoinositides to diacylglycerol or the de novo synthesis of diacylglycerol from glycerol 3-phosphate, but does involve the Ca2+-dependent conversion of phosphatidylethanolamine and phosphatidylcholine to diacylglycerol.

Animals↗