Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the qualitative and quantitative changes of ACTH-cells in the rat after application of a specific and a non-specific stimulus. A CRF-analog (lysin-vasopressin) and a prostaglandin (prostaglandin E1) were used. 40 rats were injected lysin-vasopressin or prostaglandin E1, respectively, for 4 weeks. The pituitary glands were investigated by means of light microscopy, electron microscopy and morphometry. Activation of the ACTH-cells could be observed after use of both substances, the effect of lysin-vasopressin being more intense than that of prostaglandin E1. Enlargement of the nucleus, the cytoplasm and the organelles involved in hormone-production and -transport were found and verified by morphometry. Additionally an increase in number of the cells could be demonstrated. Prostaglandin influenced not only ACTH-cells, but also other cells of the anterior pituitary.
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PMID:Ultrastructure and morphometry of ACTH-producing cell in the rat anterior pituitary gland stimulated by lysin-vasopressin and prostaglandin E1. 20 15

Production, transport, storage and release of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system were investigated. ADH produced by nerve cells in the paraventricular and supraoptic nuclei of the hypothalamus is present in a form bound to the specific protein neurophysin, in the neurosecretary granula. Electric and chemical stimulation of these nuclei results in evoked release of ADH in ionic association with neurophysin from the neural lobes. Acetylcholine, norepinephrine, histamine, angiotensin II, gamma-aminobutyric acid and L-glutamic acid have been regarded as candidates of chemical transmitters for the release of ADH in the hypothalamus. Prostaglandin (PG) E2 may be another important compound for central regulation of water metabolism. The possibility that PGE2 may be the transmitter or a modulator in the nuclei has to be considred. Serotonin, dopamine and taurine, however, may not be involded in the ADH releasing mechanisms in the hypothalamus. It appears that norepinephrine, histamine, angiotensin II, PGE2 and bradykinin stimulate directly the neural lobe to release ADH. The ADH release is regulated by intracellular Ca++. The existence of a "readily-releasable pool" of ADH can be ruled out and any limitation in the amount of ADH released under experimental conditions may be due to insufficient activation of the neural lobe. A physiological significance other than a carrier was proposed for neurophysin.
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PMID:[The hypothalamo-neurohypophysial system and antidiuretic hormone (author's transl)]. 33 45

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.
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PMID:Interactions between brain acetylcholine and prostaglandins in control of vasopressin release. 187 99

Prostaglandin (PG) inhibits the hydroosmotic effect of vasopressin. We therefore reexamined the interaction of vasopressin (VP), cAMP, and prostaglandins in toad bladder epithelial cells. Vasopressin slightly, but reproducibly, stimulated PGE2 and thromboxane B2 (TXB2) synthesis in cells prepared by the use of collagenase. When cells were prepared in the presence of a readily reversible cyclooxygenase inhibitor, ibuprofen, subsequent PGE2 synthesis was enhanced sevenfold but that of TXB2 was not. Increasing cAMP by either phosphodiesterase inhibition or 8-bromo-cAMP significantly inhibited both basal and VP-stimulated PGE2 synthesis. This inhibition was overcome by addition of arachidonic acid. Future studies employing these agents will have to consider these effects. VP enhanced 32P labeling of phosphatidylinositol (PI) and phosphatidic acid. This effect was prevented by the phosphodiesterase inhibitor, which also decreased phosphatidylcholine labeling. The results indicate that the phosphodiesterase inhibitor for cAMP may decrease PG formation by interfering with phospholipase activation. Furthermore, VP, similar to its effect in the liver, also increases PI turnover in toad bladder. This may initiate PG synthesis and provide a link among VP, cAMP, and calcium. A double-reciprocal feedback is proposed, whereby VP stimulates PG synthesis in a cAMP-independent manner and also inhibits PG synthesis in a cAMP-dependent manner.
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PMID:Interactions of vasopressin, cAMP, and prostaglandins in toad urinary bladder. 257 84

These experiments studied the effect of parathyroid hormone (PTH) (1-84) on water and Ca transport in isolated toad bladder sacs and toad bladder epithelial cells. Serosal addition of PTH significantly inhibited maximal water flow induced by vasopressin or exogenous cyclic AMP. This effect was seen over a wide range of concentrations, with the threshold for the effect occurring at 1 ng/ml. Pretreatment of the toad bladder sacs with prostaglandin inhibitors (indomethacin or ibuprofen, 1 X 10(-6) M) or preincubation in low-Ca medium (0.089 mM) abolished the effect of PTH on vasopressin-stimulated water flow. Pretreatment of the toad bladders with lanthanum (5 X 10(-5) M) also abolished the effect of PTH on vasopressin-stimulated water flow. Synthetic PTH (1-34) inhibited vasopressin-stimulated water flow only at a high concentration (1 microgram/ml). PTH increased 45Ca uptake by toad bladder epithelial cells but had no effect on 45Ca efflux. These results demonstrate that PTH inhibits water transport beyond the generation of cyclic AMP. That the effect of PTH was abolished in a low-Ca medium or by pretreatment with lanthanum suggests that cell Ca uptake is required for the effect of PTH on water transport. That prostaglandin inhibitors also block the effect of PTH on vasopressin-stimulated water flow suggests that prostaglandin synthesis is required for the effect. These data suggest that the effect of PTH on water flow is mediated by an increased cellular uptake of Ca that stimulates prostaglandin release. Prostaglandin release, in turn, appears to mediate the inhibitory effect of PTH on vasopressin-stimulated water transport.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone inhibits water flow in the isolated toad bladder. 300 14

The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and beta-endorphin-like immunoreactivity (beta-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2.8 and 28 mumol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of beta-EI was enhanced by indomethacin (28 mumol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of beta-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 mumol/l). Prostaglandin F2 alpha (5 mumol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 mumol/l) did not. Prostaglandin F2 alpha (5 mumol/l), D2 and I2 (1.5 mumol/l each) produced no effects on beta-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of beta-EI and, as can be inferred, alpha-MSH, by a direct action on intermediate lobe cells.
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PMID:Inhibition by prostaglandin E2 of the release of vasopressin and beta-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro. 316 Aug 2

Prostaglandin (PG) efflux into ureteral (UE) and venous effluents (VE) of rabbit isolated perfused kidneys was determined by superfusion bioassay and radioimmunoassay (RIA), in response to injections of arginine-vasopressin (AVP), the non-pressor vasopressin analogue 1-deamino-8-D-arginine vasopressin (dDAVP) and arachidonic acid (AA). dDAVP (10-1000 ng) failed to stimulate renal PG release, whereas AVP (10-100 ng) and AA (10-50 micrograms) caused a dose-dependent release of PG. AVP evoked PG release into both effluents with release into the VE greater than UE at high doses. In contrast, PG release by AA was almost exclusively into the VE. Indomethacin (2.8 X 10(-6) mol/l) abolished AVP- and AA-induced PG efflux in both effluents, and vasodepressor responses to AA. PGE2 was the predominant PG released in response to AVP in both effluents whereas AA released primarily 6-keto-PGF1 alpha. The contrasting sites and profile of released PG suggest that exogenous AA and AVP stimulate the release of PG from different regions/cell types within the kidney.
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PMID:Renal prostaglandin efflux induced by vasopressin, dDAVP and arachidonic acid: contrasting profile and sites of release. 379 10

The effect of prostaglandin E(1) (PGE(1)) on the water permeability response to vasopressin, theophylline, and cyclic adenosine 3',5'-monophosphate (C-AMP) of isolated, perfused collecting tubules of the rabbit was investigated in vitro. Prostaglandin is a naturally occurring substance present in a number of tissues, including kidney. It has been implicated in the action of a variety of hormones, many of which are known to exert their physiological effects through the intermediacy of the C-AMP system. In the collecting tubule, PGE(1) (10(-7) M) elicited a minimal increase in net water absorption along an osmotic gradient. However, when administered in association with a concentration of vasopressin (2.5 muU ml(-1)) selected to induce a submaximal increment in water absorption, the effect of the latter was reduced by approximately 50%. Theophylline (5 x 10(-3) M) also increased net water absorption, an effect not previously demonstrated in renal tissue. This effect was potentiated by the simulataneous addition of PGE(1). In contrast, PGE(1) did not influence the increase in net water absorption induced by C-AMP (10(-2) M). Since C-AMP is responsible for the permeability effects of vasopressin in renal tissue, the present results are consistent with the view that PGE(1) interferes with the action of the octapeptide by competing with it at a site which influences the generation of C-AMP. In addition it is proposed that prostaglandin may be an important modulator of the action of vasopressin. The tubule is exquisitely sensitive to the hormone, responding to as little as 0.25 muU ml(-1). It is conceivable that in the intact animal prostaglandin may serve to dampen the effects of small amounts of residual hormone and thereby prevent overshoots in permeability which might otherwise occur.
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PMID:Effect of prostaglandin E1 on the permeability response of the isolated collecting tubule to vasopressin, adenosine 3',5'-monophosphate, and theophylline. 429 82

1. Prostaglandin E(1) increases sodium transport as measured by short circuit current (SCC) across isolated frog skin whereas calcium, added to the external Ringer fluid, decreases sodium transport. To help establish the site of action of prostaglandin the possible interaction of these two agents on sodium transport has been examined.2. The effect of a standard dose of prostaglandin (0.5 x 10(-6)M) on the short circuit current was tested on paired skins with either zero or high calcium (22.4 mM) in the external Ringer fluid. In ten experiments the responses to prostaglandin (expressed in muA/cm(2)) were not significantly affected by external calcium.3. In another series of experiments the chelating agent, EGTA, was included in calcium-free external Ringer in order to promote greater depletion of skin calcium. The response of these skins to the standard dose of prostaglandin was of the same order of magnitude as that of control skins. The response was not sustained in contrast to that of normal skins and skins in high-calcium fluids.4. In a further series of experiments the reverse procedure was adopted whereby the response of the skin to low and high doses of calcium in the external Ringer was recorded in control conditions and when the skin had responded fully to twice the standard dose of prostaglandin. In addition, the calcium-sensitive current was calculated for each skin in both circumstances. The latter was unchanged on addition of prostaglandin, and graded doses of calcium caused the same degree of inhibition of the short circuit current.5. The results show no interaction between external calcium and prostaglandin and also no need for external calcium in prostaglandin stimulation of sodium transport.6. The findings do not support the concept of chelation by prostaglandin of calcium from critical sites on the skin as the primary mechanism of its action on sodium transport. The results closely parallel those of a similar type of study into the relationship between vasopressin and external calcium on frog skin also.7. When frog skin has responded fully to either prostaglandin E(1) or vasopressin, it shows no response to the other, although removal of calcium from the external Ringer fluid causes a further increase in short circuit current.8. Vasopressin causes a further increase in short circuit current in skins treated with prostaglandin F(1alpha). Prostaglandin F(1alpha) may be a weaker agonist on frog skin than either vasopressin or prostaglandin E(1).
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PMID:Effect of calcium and vasopressin on the response of frog skin to prostaglandin E1. 454 93

Prostaglandin (PG) production by the kidney is known to be reduced both in vivo and in vitro in rats with hereditary diabetes insipidus (DI), totally lacking ADH. Exogenous ADH restores normal PG excretion in these rats. On the other hand, osmolality in vitro, and urine flow rate in vivo have been shown to influence PG synthesis rate. In order to determine whether the decreased PG synthesis of DI rats is due to the lack of antidiuretic hormone itself or to low tissue osmolality, we studied in vivo and in vitro PG production in DI rats in which urine osmolality had been raised either with ADH (infused by Alzet minipumps), or without ADH (by dehydratation) and in control DI rats. PGE2 and PGF2 alpha were measured by radioimmunoassay in the urines and in supernatants of papillary homogenates incubated at 37 degrees C for 15-120 min. ADH administration and dehydration led to similar urine osmolalities (congruent to 900-1,000 mosmol/kg H2O versus 150 in controls). However, only ADH administration but not dehydration increased PG urinary excretion (X 5, P less than 0.001) and subsequent in vitro papillary synthesis (X 1.6, P less than 0.01). These results show that antidiuretic hormone increases PG-synthesis of the renal papilla directly and not through its effects on papillary osmolality.
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PMID:Effects of osmolality and antidiuretic hormone on prostaglandin synthesis by renal papilla. Study in Brattleboro rats with diabetes insipidus. 670 93


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