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PubMed1985

The lack of 'sensitization' to the pressor effects of centrally injected vasopressin in rats.

Vasopressin causes motor disturbances following intracerebroventricular injections and a second central injection results in an apparent sensitization of the animal to the convulsant effect of vasopressin. In this study, the effect of vasopressin pretreatment on the central and peripheral pressor effects of vasopressin was examined in Sprague-Dawley rats. There was no increase in the responsiveness to the pressor effects of vasopressin, either central or peripheral, in animals that had previously received central vasopressin. This evidence suggests that the phenomenon of increased sensitivity to vasopressin is not displayed by all vasopressin's actions.

Animals↗
PubMed1988

Direct excitatory action of vasopressin in the lateral septum of the rat brain.

The electrophysiological action of arginine vasopressin on neurones in the lateral septum of the rat brain was studied using extracellular recordings and the in vitro brain slice technique. Of 177 neurones tested in the presence of vasopressin at 1-1000 nM, 77 (about 44%) responded by a reversible increase in firing rate, 12 (about 7%) were inhibited and the remaining were not affected. The lowest peptide concentration effective in exciting septal neurones ranged between 1 and 50 nM, and the magnitude of the excitatory effect was concentration dependent. At high vasopressin concentrations, the peptide-induced excitation was often followed by a transient pause in firing; this was probably due to action potential inactivation, brought about by the vasopressin-induced neuronal membrane depolarization. The excitatory effect of vasopressin was postsynaptic, since it was not abolished following synaptic blockade in a low calcium-high magnesium perifusion solution. A comparison of the effects of vasopressin and oxytocin suggested that most of the septal vasopressin-sensitive neurones are endowed with vasopressin receptors, whereas a minority of them bear oxytocin receptors.

Action Potentials↗
PubMed1991

Amygdala kindling elevates plasma vasopressin.

Acute and chronic effects of epilepsy on endocrine function are known to occur in humans with partial seizures of limbic origin and in animals with limbic kindled seizures. The amygdala, a component of the limbic system, has dense hypothalamic connections and amygdala stimulation in monkeys and cats result in vasopressin release. In the present study we sought to determine if amygdala stimulation in the rats results in an immediate acute release of vasopressin and to determine if acute or chronic changes occur in vasopressin release in the fully kindled animal. Plasma vasopressin, osmolality and hematocrit were measured in blood samples drawn from rats with implanted venous catheters before and after stimulation and at different stages of kindling. Low-frequency (15 Hz) electrical stimulation of the amygdala was followed by an immediate, 3-fold increase in plasma vasopressin concentration. Moreover, although the 60 Hz kindling stimulus did not result in a significant immediate rise in plasma vasopressin prior to kindling, after kindling to stage 5 seizures the 60 Hz kindling stimulus resulted in seizures and a significant immediate rise in plasma vasopressin. In addition, we found that kindling was followed by a significant, though modest, rise in the resting plasma vasopressin without an accompanying change in osmolality or hematocrit. We conclude that kindling results in a persistent alteration in the vasopressinergic neuroendocrine system.

Amygdala↗
PubMed1993

Fluoxetine induces vasopressin and oxytocin abnormalities in food-restricted rats given voluntary exercise: relationship to anorexia nervosa.

Anorexia nervosa is associated with vasopressin, oxytocin and serotonin abnormalities. Because of the relationship between exercise and anorexia nervosa, we explored the weight-loss syndrome produced by wheel running in food-deprived rats. Its effects on regional vasopressin and oxytocin concentrations were determined under basal conditions and following systemic fluoxetine. Weight-matched, exercised and unexercised rats served as controls. Fluoxetine caused abnormalities in suprachiasmatic vasopressin and dynorphin A content and in thymus oxytocin content that did not occur in weight-matched or exercised controls. No syndrome-specific anomalies occurred in the hypothalamo-neurohypophysial system or dorsal vagal complex (DVC). However, weight reduction and fluoxetine increased circulating vasopressin; moderate exercise caused fluoxetine-induced elevations in posterior pituitary vasopressin and oxytocin; and, unlike the other groups, fluoxetine increased DVC oxytocin in freely fed unexercised rats. It was concluded that syndrome-specific vasopressin and oxytocin abnormalities occur that are not secondary to weight loss or moderate exercise; that weight loss or fluoxetine increases circulating vasopressin; that moderate exercise alters neurohypophysial vasopressin and oxytocin content; and that weight loss or exercise inhibits a fluoxetine-stimulated increase in DVC oxytocin. Finally, it was argued that the fluoxetine abnormalities indicate possible serotonin dysfunction in the syndrome.

Animals↗
PubMed1988

Vasopressin and adrenalectomy-induced sensitivity to morphine.

Arginine vasopressin, vasopressin antiserum and a specific vasopressin pressor antagonist were injected intracerebroventricularly into adrenalectomized rats before morphine-induced antinociception was tested. In these experiments we have exploited previous findings which showed that the antinociceptive effect of opioids was potentiated after adrenalectomy; rats that were adrenalectomized in the morning under basal resting conditions of the pituitary-adrenal system displayed significantly higher response latencies after morphine administration than rats adrenalectomized in the evening. These effects were measured 7 days after adrenalectomy. The same conditions were used in this study. Both, the vasopressin antiserum and the vasopressin antagonist abolished the morning adrenalectomy-induced hypersensitivity to centrally injected morphine and were not effective when administered to rats that had been adrenalectomized in the evening. The reverse was observed after intraventricular administration of vasopressin. The peptide significantly raised the sensitivity to morphine-induced antinociception of rats that had been adrenalectomized in the evening whereas it did not affect antinociception in animals that had been adrenalectomized in the morning. Vasopressin levels determined by radioimmunoassay in the cerebrospinal fluid were significantly higher in adrenalectomized animals. We propose that vasopressin is a critical neuropeptide factor involved in the adrenalectomy-induced hypersensitivity to morphine antinociception.

Adrenalectomy↗
PubMed1996

Contractile responses of human deferential artery and vas deferens to vasopressin.

We studied the effects of vasopressin on isolated rings of human deferential artery and vas deferens (prostatic portion) obtained from patients undergoing radical cystectomy (n = 11) or prostatectomy (n = 10). Ring segments of artery or vas deferens were studied in organ bath experiments at optimal resting tension. In artery rings, vasopressin produced concentration-dependent, endothelium-independent contractions with an EC50 of 4.5 x 10(-10) M. The presence of NG-nitro-L-arginine methyl ester hydrochloride (10(-4) M), an inhibitor of nitric oxide synthase, did not change significantly (P > 0.05) the vasopressin-induced contraction. In ring preparations of the prostatic part of the vas deferens, vasopressin induced phasic contractions with an EC50 of 7.0 x 10(-9) M. The vasopressin V1 receptor antagonist, d(CH2)5Tyr(Me)AVP (10(-8) and 10(-6)), displaced to the right in parallel the control curve to vasopressin in artery and vas deferens rings. These results indicate that vasopressin exerts a powerful constrictor action on human deferential artery and vas deferens by direct stimulation of V1 receptors. It is concluded that the deferential artery may dampen the passage of blood to the vas deferens in circumstances characterized by increased plasma vasopressin levels.

Aged↗
PubMed1984

Inhibition by somatostatin of the vasopressin-stimulated adenylate cyclase in a kidney-derived line of cells grown in defined medium.

LLC-PK1L cells, a kidney-derived cell line grown in defined medium, possess a vasopressin-sensitive adenylate cyclase. Somatostatin was able to inhibit the vasopressin-induced increase in adenylate cyclase activity, without affecting the basal enzyme activity. This inhibition was competitive. No effect of somatostatin could be detected on [3H]vasopressin binding suggesting an interaction of somatostatin with the vasopressin-sensitive system distal to the hormone-receptor interaction. At variance with N6-L-2-phenylisopropyladenosine (PIA), GTP did not potentiate the inhibition by somatostatin. The inhibition of the vasopressin stimulation by somatostatin and that by PIA were additive. Changing the composition of the cell growth medium increased the number of vasopressin receptors per cell. Cells with a high number of vasopressin receptors were less sensitive to inhibition by somatostatin. Such results suggested that somatostatin and vasopressin receptors and/or the inhibitory (Ni) and stimulatory (Ns) regulatory transducing components are regulated by different mechanisms.

Adenylyl Cyclases↗
PubMed1987

Hyposensitivity to vasopressin in a hemorrhaged-transfused rat model of portal hypertension.

This study was designed to evaluate the hemodynamic response to vasopressin infusion during hemorrhage and blood transfusion in a rat model of portal hypertension. Portal pressure, arterial pressure, and regional and systemic blood flows were measured in a rat model of portal hypertension receiving placebo or vasopressin infusion. Effects of the drugs were compared in control rats and rats subjected to hemorrhage and blood transfusion. In a stable portal hypertensive rat group (no hemorrhage or transfusion) a standard vasopressin dose, 2.5 mU X kg-1 X min-1, resulted in a significantly lower portal pressure (11.5 +/- 0.7 vs. 14.4 +/- 0.6 mmHg) with a concomitantly lower portal venous inflow (8.5 +/- 0.3 vs. 11.1 +/- 0.6 ml X min-1 X 100 g body wt-1) when compared with rats receiving placebo. These findings are in contrast to the effects obtained with the same dose of vasopressin given during blood transfusion to hemorrhaged portal hypertensive rats. The standard dose of vasopressin had no effect on any of the splanchnic or systemic circulatory parameters. Only when a dose of vasopressin 10 times larger was used in the hemorrhaged-transfused animals were hemodynamic effects noted. A significant decrease in portal flow and pressure was noted. These findings suggest that vasopressin given during hemorrhage may be less effective than when given during a stable state. Larger doses of vasopressin may be needed during hemorrhage to produce the same effect as seen during a controlled stable state. Caution should be used in extrapolating the results of pharmacologic studies in stable portal-hypertensive models to hypovolemic states in humans.

Animals↗
PubMed1983

Vasopressin affects adenylate cyclase activity in rat brain: a possible neuromodulator.

The effect of vasopressin on adenylate cyclase activity was measured in the homogenates of selected rat brain regions. Adenylate cyclase activity in homogenate of the caudate nucleus did not change significantly with various concentrations of vasopressin. Furthermore, vasopressin did not reliably alter adenylate cyclase activity in various brain regions. Vasopressin in low concentrations significantly enhanced the activation of caudate adenylate cyclase activity by dopamine. This effect of vasopressin was dose dependent. Maximal enhancement by vasopressin occurred at 100 microM vasopressin. These results indicate that vasopressin may not have a direct effect on brain adenylate cyclase activity but appears to modulate the action of dopamine on brain adenylate cyclase.

Adenylyl Cyclases↗
PubMed1993

Characterization of vasopressin-mediated GSH efflux from Hep G2 cells: significance of protein kinase C.

Vasopressin stimulated GSH efflux from Hep G2 cells. The maximal effect was observed at 10nM. Pretreatment with pertussis toxin or cholera toxin for 18 hr increased GSH efflux. Vasopressin-mediated GSH efflux was observed even in the cells pretreated with those compounds. Dibutyryl-cAMP or dibutyryl-cGMP enhanced GSH efflux although an additive effect of vasopressin was not observed. Glucagon and a phorbol ester independently increased GSH efflux while both compounds decreased the effect of vasopressin. Staurosporine, an inhibitor of protein kinase C, inhibited vasopressin-mediated GSH efflux. The effect of vasopressin was observed even in the absence of extracellular Ca2+. Vasopressin stimulates GSH efflux from Hep G2 cells and protein kinase C-dependent pathway may play a significant role in vasopressin-mediated GSH efflux.

Alkaloids↗
PubMed1991

Chronic ethanol exposure uncouples vasopressin synthesis and secretion in rats.

To assess the chronic effect of ethanol on vasopressin release and synthesis, hypothalamic vasopressin mRNA, plasma vasopressin levels and plasma osmolality were measured in control rats and rats exposed chronically to ethanol by vapor inhalation for 8 days. The level of hypothalamic vasopressin mRNA (vasopressin synthesis) was unchanged or significantly decreased in ethanol-treated rats, even when these animals displayed increased plasma osmolality and vasopressin levels. The results suggest that chronic ethanol exposure produces a down-regulation of vasopressin synthesis and/or a disruption of vasopressin synthesis-secretion coupling. These findings may have important implications for evaluation of the hydration state of chronic alcoholics.

Animals↗
PubMed1991

Vasopressin stimulates pyruvate utilization through a Ca(2+)-dependent mechanism and lactate formation by a protein kinase C-dependent mechanism in isolated rat hepatocytes.

Vasopressin stimulates lactate production by hepatocytes from fed rats, an effect which has been attributed exclusively to Ca2+ activation of glycogenolysis. We provide evidence here for two further actions of vasopressin which affect lactate formation by rat hepatocytes. In the presence of 50 mM glucose, vasopressin inhibited lactate production by hepatocytes. The inhibition was relieved by the presence of alpha-cyano-4-hydroxycinnamate (alpha-CHC), which blocks mitochondrial pyruvate transport. This suggests that vasopressin stimulates pyruvate utilization in the presence of a high concentration of glucose. Epidermal growth factor (EGF), which also increases lactate formation by hepatocytes, did not similarly decrease lactate accumulation in the presence of high glucose, suggesting no stimulation of lactate and pyruvate utilization by this hormone. In cells depleted of Ca2+, vasopressin also stimulated lactate formation. Although vasopressin did not cause the apparent translocation of protein kinase C between cell spaces, phospholipase C treatment of hepatocytes did duplicate vasopressin stimulation of lactate formation, provided fatty acid oxidation was suppressed by the simultaneous presence of the inhibitor palmixorate. We conclude that three actions of vasopressin affect lactate and pyruvate formation: the calcium-linked activations of glycogenolysis and mitochondrial pyruvate utilization, and a stimulation of glycolysis likely mediated by protein kinase C.

Adenosine Triphosphate↗
PubMed1990

Arginine vasopressin induces the expression of c-fos in the mouse septum and hippocampus.

Arginine vasopressin is a neuropeptide that has been shown to modulate functional ethanol tolerance and memory processes. These actions of vasopressin in the CNS have been shown by us and others to be mediated by V1 receptors. Intracerebroventricular injection of vasopressin in mice resulted in a substantial increase in mRNA for the proto-oncogene c-fos in septum and hippocampus, but no increase in cerebral cortex. A V1-selective agonist also increased septal c-fos mRNA levels, while a V2-selective agonist was less effective. Similarly, the response to vasopressin was more effectively blocked by a V1- than a V2-selective antagonist. These results indicate that vasopressin acts specifically at V1 receptors in mouse septum and hippocampus to increase c-fos mRNA. The vasopressin metabolite, AVP(4-9), also increased c-fos mRNA levels in septum and hippocampus, while the response to oxytocin, which has different effects from vasopressin on memory and tolerance, was greater in hippocampus than in septum. Nerve growth factor, in contrast to the other peptides, had a more pronounced effect on c-fos mRNA levels in cerebral cortex than in the other brain areas. Increased c-fos expression has been hypothesized to play a role in neuroadaptation, and these results suggest that modulation of septal c-fos expression could be important for vasopressin effects on ethanol tolerance and/or memory.

Animals↗
PubMed1980

Ontogeny of vasopressin and oxytocin in the fetal rat: early vasopressinergic innervation of the fetal brain.

The content and distribution of vasopressin and oxytocin were determined during fetal development in the rat brain and pituitary by means of radioimmunoassay and immunocytochemistry. The vasopressin content in the fetal brain showed a gradual rise from day 16 of pregnancy onwards, while pituitary vasopressin rapidly increased from fetal day 19 until birth. The oxytocin content in the fetal brain was considerably lower than the vasopressin content. A decrease in oxytocin content was seen between day 16 and day 18 while from day 18 of pregnancy onwards a slight increase was found. The pituitary oxytocin content starts to rise between day 17 and 18 of pregnancy, but at term the pituitary oxytocin content was only 1/20 of the vasopressin value. Immunocytochemistry revealed that vasopressin levels in the fetal rat brain were not only due to the presence of the classical hypothalamoneurohypophyseal system, but also to the early development of exohypothalamic fibers. Vasopressin containing cells were seen from fetal day 16 in the supraoptic nucleus, and from fetal day 18 in the paraventricular nucleus. The fiber outgrowth of these cells towards the pituitary and extrahypothalamic brain sites seems to be well synchronized, as on day 17 vasopressin containing fibers could be demonstrated in the olfactory bulb as well as in the median eminence. No positive staining for oxytocin could be obtained in the fetal rat, while during the entire fetal period no positive staining was found in cell bodies in the region of the suprachiasmatic nucleus. The early peptidergic innervation of the brain, which enabled the tracing of the source of some exohypothalamic fibers, might be related to several central processes among which brain development itself is included.

Animals↗
PubMed1984

Synaptic input to vasopressin neurons of the paraventricular nucleus (PVN).

Following injections of horseradish peroxidase into the PVN, retrogradely filled cells were found in regions of the limbic system known to contain glucocorticoid concentrating neurons [4, 31, 44]. To determine if these regions which include the lateral septum, medial amygdala and ventral subiculum have a monosynaptic input to vasopressin neurons we developed a double label ultrastructural technique [20] to simultaneously visualize immunoreactive neuropeptide and anterogradely transported HRP. Following injections of tracer into all three of these regions, HRP labeled fibers were seen at the light microscopic level to form a halo in the perinuclear, cell poor zone around the PVN. Ultrastructural examination of this area resulted in the discovery of a small number of limbic system synapses on vasopressin dendrites. These synapses were most numerous in the ventral and medial portion of the cell poor zone. A similar pattern of innervation was seen for the supraoptic and suprachiasmatic nucleic which also contain vasopressin cells whose dendrites extend beyond the nuclear boundaries. In a similar fashion we were interested in determining the distribution of noradrenergic terminals on vasopressin neurons in the various subnuclei of the PVN. We have combined immunocytochemistry for vasopressin with radioautography for 3H-norepinephrine (NE) at the ultrastructural level. NE terminals were numerous in the periventricular zone, innervating both vasopressin containing dendrite and non-immunoreactive dendrites and cell bodies. The vasopressin dendrites could originate from cells either resident in the periventricular zone or from cells situated in more lateral subnuclei. In the main, lateral magnocellular region, noradrenergic terminals were very few in number and innervated almost exclusively non-vasopressin containing structures. These studies demonstrate the need for ultrastructural analysis of synaptic input to neurosecretory cells.

Animals↗
PubMed1980

Effect of vasopressin on cyclic AMP-dependent protein kinase in toad urinary bladder.

The effect of vasopressin on the toad urinary bladder has been shown to be mediated by cyclic AMP. It has been assumed that, as demonstrated for other systems, this involves activation of cyclic AMP-dependent protein kinase. In order to test this hypothesis we investigated the effect of vasopressin on cyclic AMP-dependent protein kinases in epithelial cells of toad bladders. About 80% of protein kinase activity and cyclic AMP-binding capacity was found to be in the cytosol. DEAE-cellulose chromatography showed a pattern of 15--20% type I and 80--85% type II cyclic AMP-dependent protein kinase. Cytosolic kinase was activated 3--4-fold by cyclic AMP with half-maximal activation at 5 . 10(-8) M. Similarly, half-maximal binding of cyclic AMP occurred at 7 . 10(-8) M. Incubation of toad bladders in Ringer's solution containing 0.1 mM 3-isobutyl-1-methylxanthine, prior to homogenization and assay, showed stable cyclic AMP-binding capacity and protein kinase ratio --cyclic AMP/+cyclic AMP. Exposure of bladders to 10 mU/ml of vasopressin for 10 min caused intracellular activation of protein kinase and decrease in cyclic AMP-binding capacity that were maintained for at least 30 min. Incubation of bladders with increasing concentrations of vasopressin (0.5--100 mU/ml) resulted in a discrepancy between a progressive increase in cyclic AMP levels and a levelling off at 10 mU/ml of vasopressin for the changes in protein kinase ratio and cyclic AMP-binding capacity. The increase in kinase ratio was due to higher activity in the absence of exogenous cyclic AMP and was fully inhibitable by a specific protein kinase inhibitor. Using Sephadex G-25-CM50 column chromatography for separation of holoenzyme and free catalytic subunit we demonstrated that the activation of protein kinase in the vasopressin-treated bladders is due to intracellular dissociation of the kinase. These results show that the effect of vasopressin on the toad bladder involves activation of a cytosolic cyclic AMP-dependent protein kinase. The time course and the dose-response curve of the kinase activation closely parallel vasopressin's effect on osmotic water flow.

Animals↗
PubMed1984

Vasopressin and oxytocin in the rat spinal cord: distribution and origins in comparison to [Met]enkephalin, dynorphin and related opioids and their irresponsiveness to stimuli modulating neurohypophyseal secretion.

Immunoreactive-vasopressin, -oxytocin, -dynorphin, -dynorphin-(1-8), -alpha-neo-endorphin and -[Met]enkephalin were, in each case, present in greater concentrations in dorsal as compared to ventral, and lumbo-sacral as compared to cervico-thoracic, spinal cord. These differences were significantly more pronounced for vasopressin and oxytocin than for the other peptides. Lesions of the hypothalamic paraventricular nucleus depleted levels of immunoreactive-vasopressin and -oxytocin throughout the cord whereas levels of the opioid peptides therein were unaffected. In contrast, destruction of either the supraoptic or suprachiasmatic nucleus failed to change the content of immunoreactive-vasopressin, -oxytocin or any of the opioid peptides in the cord. Dehydration for 3 days depressed levels of immunoreactive-vasopressin, -oxytocin and -dynorphin in the neurointermediate lobe of the pituitary. In distinction, the levels of these were not modified in the spinal cord. Further, treatment with the synthetic corticosteroid, dexamethasone, elevated levels of immunoreactive-vasopressin, -oxytocin and -dynorphin in the neurointermediate pituitary whereas these were unaffected in the spinal cord. It is concluded that vasopressin and oxytocin in the spinal cord are predominantly derived from the paraventricular nucleus, localized in dorsal lumbo-sacral regions of the cord and insensitive to endocrinological manipulations. These pools may, thus, be modulated differently from their counterparts in the neurohypophysis and have a differing role, possibly in the control of the primary processing, autonomic or motor junctions. Further, there is no evidence from these or our prior studies for a close interrelationship of spinal cord vasopressin with dynorphin-related peptides (or oxytocin with [Met]enkephalin), likewise in contrast to the neurohypophysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Vasopressin neuron survival in neonatal Brattleboro rats; critical factors in graft development and innervation of the host brain.

Previously it was found that grafts of supraoptic plus paraventricular areas from 19-day-old foetal normal rats survived in the third ventricle of the brain of 4- to 6-day-old, vasopressin-deficient Brattleboro pups, but could not alleviate their polyuria. In the present series, factors important in graft development were analysed. Again using day-19 fetuses as donors, anterohypothalamus grafts as well as grafts placed near a crushed median eminence survived relatively poorly, but showed the presence of vasopressin neurons immunocytochemically one month post-grafting. Homotopic grafting in the supraoptic nucleus, however, even failed to show surviving vasopressin neurons. Graft survival was improved by the use of donor tissue of fetuses younger than day 19. Parvocellular vasopressin cells were frequently seen, organized into clusters resembling the normal suprachiasmatic nucleus. However, magnocellular neurons, as normally seen in supraoptic and paraventricular nuclei, only survived grafting when taken between days 11 and 15 of fetal age. It was concluded that only immature vasopressin neurons survived grafting under the condition employed. Magnocellular neurons had a limited fiber outgrowth into the host brain and median eminence. Most large neurons only stained with non-specific neurophysin antiserum, not with specific vasopressin-associated neurophysin antiserum. Thin fibers of the parvocellular vasopressin neurons provided only occasional and sparse innervation of the host median eminence and lateral septum (one case), but several examples of massive fiber bundles running dorsally from graft into host brain were observed. These fibers terminated in the thalamic periventricular area, a nucleus that is normally innervated by the vasopressin neurons of the suprachiasmatic nucleus. The failure of the grafts to provide adequate vasopressinergic innervation of the host median eminence probably explains why none of the nearly 200 Brattleboro neonates operated upon showed any sign of relief of their diabetes insipidus. It suggests, however, that the present procedures might be useful in restoring central vasopressinergic functions in the developing Brattleboro rat.

Aging↗