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 regulation of cytoplasmic calcium is a key process in nerve tissue. Using a smooth muscle model we have shown that prostaglandin (PG) E2 probably regulates entry from extracellular fluid, whereas the release from intracellular stores depends on the interplay between thromboxane (TX) A2, PGEI and prostacyclin. Hormones and other agents interact with this system in the following ways: vasopressin, angiotensin and inositol mobilize arachidonic acid from membrane phospholipids and increase synthesis of PGE2 and TXA2, cortisol blocks this action. Prolactin and zinc mobilize dihomo-gamma-linolenic acid and increase synthesis of PGEI. These effects can be blocked by cortisol, lithium and taurine, three agents which on their own have no effect on basal PG production. Epileptogenic agents like penicillin and picrotoxin also stimulate PG synthesis, while diphenylhydantoin is a PG antagonist and diazepam is a TXA2 antagonist. The effects of all these agents occur at concentrations which are physiological in the case of the natural ones, and readily attained in human plasma in the case of the drgus. In view of recent evidence that calcium may be important in demyelination and considering the established role it plays in nerve conduction and synaptic transmission, we suggest that these observations may be of significance in understanding Friedreich's ataxia.
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PMID:Regulation of cytoplasmic calcium: interactions between prostaglandins, prostacyclin, thromboxane A2, zinc, copper and taurine. 34 85

To determine whether hypothalamic function is normal in patients with idiopathic gonadotrophin deficiency, nine men with this syndrome were studied. Water conservation after overnight dehydration, thermoregulatory response to a cold (10 degrees C) environmental stress and prolactin secretion following chlorpromazine stimulation were investigated. In response to dehydration, maximal urinary osmolality was 1058 +/- 135 mOsm/kg (mean +/- SD) and no patient showed further increase after exogenous vasopressin administration. The patients responded to the cold stimulus by vigorous shivering and maintained their core body temperatures. Basal concentrations of prolactin which were 12.7 +/- 4.6 ng/ml increased by 15 ng/ml following Thyrotrophin-releasing hormone in six of seven men tested, indicating normal pituitary reserve. Prolactin concentrations doubled in seven of eight men who received chlorpromazine. All responses were indistinguishable from those of normal men. While a diminished secretion of gonadotrophin releasing hormone by the hypothalamus remains the most plausible cause of idiopathic gonadotrophin deficiency, our data indicate that the associated functions tested are intact in men with this syndrome.
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PMID:Hypothalamic function in men with hypogonadotrophic hypogonadism. 34 48

Extracts of porcine hypothalamic fragments (HF) bring about the release of prolactin when injected into estrogen-progesterone pretreated male rats. To determine the extent to which this prolactin-releasing activity (PRA) is attributable to thyrotropin-releasing hormone (TRH) and/or vasopressin (VP), (both hormones capable of releasing prolactin in this preparation), PRA was assayed following destruction of TRH and VP by incubation in rat serum, and after separation on Sephadex G-25 columns. Acetic acid (2N) extracts of HF contain 22 to 27 ng TRH and 650 to 1000 ng of VP per HF as determined by immunoassay. Incubation for 1 h in fresh rat serum degraded 91 to 99% of both TRH and VP. PRA fell after incubation, but was still detectable, indicating residual activity that resisted degradation. Prolactin release responses to HF extracts and to TRH were log-dose dependent, but had different activity slopes. The minimal detected dose of TRH which released prolactin was 10 ng, while minimal effective doses of serum inactivated HF extract contained only 0.6 ng of TRH. Maximum effects with serum-inactivated HF extract were achieved with 2 HF equivalents containing 2.6 ng of TRH. More than 400 ng of TRH were required to give an equivalent PRA response. Sephadex G-25 chromatography of hypothalamic extracts using 2.0 N acetic acid separated a fraction which after treatment with serum to inactivate most TRH present caused marked prolactin release and contained only 0.7 ng of TRH and 0.3 ng of VP per dose. Evidence for a PIF was the demonstration that retarded fractions from the column significantly decreased plasma prolactin levels. The finding of PRA in hypothalamic extracts separate from both TRH and VP is evidence for the existence of a distinct prolactin-releasing factor.
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PMID:Prolactin-releasing factor (PRF) in porcine hypothalamic extract distinct from TRH. 82 45

Prolactin appears to play a role in osmoregulation of fishes and birds and a possible contribution of this hormone to the regulation of salt and water excretion in mammals has been suggested as well. The present studies were undertaken to investigate the role of osmotic pressure on the secretion of prolactin and the effect of the hormone on renal water excretion in man. The i.v. administration of synthetic thyrotropin releasing hormone (TRH) (7 mug/kg) to five subjects undergoing a maximal sustained water diuresis increased serum prolactin to supraphysiologic levels in all as mean concentration rose from 30.2 +/- 2.9 to 60.2 +/- 5.0 ng/ml (P less than 0.005). This increase was not associated with either significant alterations in renal hemodynamics or sodium excretion and water excretion. The osmoregulation of prolactin release was then investigated by the oral administration of 20 ml/kg of water to seven subjects in 11 studies. While the water load decreased serum osmolality from 293 +/- 285 +/- 1.5 mOsm/kg H2O (P less than 0.001), there was no significant change in prolactin level, 28+/- 1.8 to 30 +/- 2.4 ng/ml. Serum hypertonicity was achieved in six subjects with the infusion of 5% NaCl which increased serum osmolality from 287 +/- 1.8 to 298 +/- 1.4 mOsm/kg (P less than 0.001). While the hypertonic state caused a marked antidiuresis as urinary osmolality rose from 62 +/- 5.9 to 480 +/- 48 mOsm/kg (P less than 0.001), the concentration of prolactin remained unchanged at 28 ng/ml. We conclude that supraphysiologic levels of prolactin have no antidiuretic properties in a vasopressin-free state and that acute alterations in serum tonicity within the range observed do not affect the release of prolactin in man.
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PMID:Osmotic control of prolactin release and its effect on renal water excretion in man. 82 58

Prolactin was shown to activate adenylate cyclase in broken cellular enzyme preparations from rat renal medulla. Likewise, vasopresin was effective on this enzyme system. Parathyroid hormone was similarly active in the renal cortex. The simultaneous administration of vasopressin and prolactin to medullary kidney slices did not result in an additive effect in stimulating medullary adenyl cyclase. Audioradiographic techniques revealed a selective and prolonged localization of intravenously injected 125I-prolactin to the thick limb of the loop of Henle, the distal tubule and the collecting duct. It is concluded that prolactin activates medullary adenylate cyclase, and may do so by occupying ADH receptors.
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PMID:Prolactin-induced stimulation of rat renal adenylate cyclase and autoradiographic localization to the distal nephron. 86 55

Prolactin is an important osmoregulatory hormone in several lower vertebrate species. The present study was undertaken to clarify the effects of prolactin, if any, on human renal function. Eight normal adult male subjects on a 150 mEq sodium (Na), 60 mEq potassium (K) diet for 5 days were studied during 12 h of oral water (H2O) loading on 2 consecutive days. On day 1, after a 6 h control period, a 1 ml normal saline placebo was given im; on day 2, 25 mg of ovine prolactin (OP) was substituted. The subjects were supine and received a constant infusion of Na and K. After OP, serum prolactin rose from 6.9+/-0.8 ng/ml to 15.0+/-2.5 ng/ml (P less than .01) at 1 h, 27.6+/-4.0 ng/ml (P less than .002) at 2 h, 33.1+/-4.3 ng/ml (P less than .001) at 3 h and remained elevated for the remaining 3 h of study. The ovine prolactin had 20-25% of the potency of human prolactin in the human prolactin radioimmunoassay system. In response to OP, free H2O clearance (CH2O) promptly decreased from 10.1 +/- .06 ml/min to 6.1 +/- .05 ml/min (P less than 0.1) at 1 h, to a nadir of 5.1+/-.3 ml/min (P less than .001) at 2 h, and returned to control levels by 4 h. CH2O was unchanged after placebo, and urinary Na and K excretion, creatinine and osmolar clearance (COSM), plasma Na, K, osmolality and aldosterone were unchanged after OP or placebo. Control plasma vasopressin was 1.0+/-0.1 micronU/ml and was not changed after prolactin (1.1+/-0.1 micronU/ml at 1 h, 1.1+/-0.1 micronU/ml at 2 h and 1.1+/-0.1 micronU/ml at 3 h). The ovine prolactin contained 2 micronU of immunoassayable vasopressin per microng of powder. Aqueous vasopressin, 50 mU (containing in 25 mg of ovine prolactin), produced a decrease in CH2O not significantly different from prolactin in 6 water loaded subjects. Four different subjects given 100 mg of OP had decreased CH2O from 8.3+/-0.3 to 2.7+/-0.7 ml/min at 1 h (P less than .001) and to 2.8+/-0.7 ml/min at 2 h (P less than .01). Control plasma osmolality was 301+/-4 mOsm/1 and decreased to a maximum of 288+/-5 mOsm/1 4 h after OP (P less than .001). After prolactin administration, plasma vasopressin rose from 0.44+/-0.15 to 0.80+/-0.41 micronU/ml (P =NS) at 1 h. The transient antidiuresis in response to ovine prolactin is due to contamination of the preparation with vasopressin. Prolactin does not acutely influence renal electrolyte excretion and probably does not influence water excretion in man.
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PMID:The effects of ovine prolactin on water and electrolyte excretion in man are attributable to vasopressin contamination. 87 May 13

The influence of administration of ovine prolactin in vivo on intestinal fluid and ion transport in vitro was investigated using intact and hypophysectomized male rats. Prolactin administration significantly stimulated fluid, sodium,potassium, calcium, magnesium and chloride transport across everted jejunal sacs. The last two ions were affected less than the others. Hypophysectomy caused a significant decrease in fluid and sodium absorption, but prolactin treatment for 2 days restored normal absorption rates but not uniformly in all sacs. Prolactin action on fluid and sodium absorption showed a dose-dependent tendency, maximal stimulation resulting from administration of 1.0 to 2.0 mg prolactin daily; higher doses failed to elicit significant response. The stimulatory action of prolactin was inhibited by a simultaneous administration of vasopressin which when given alone had no effect on intestinal absorption. In the absence of glucose or in the presence of phlorizin, fluid transport was inhibited, the reduction being more dramatic in the presence of phlorizin. Similarly, either application of ouabain or partial replacement of sodium with isotonic choline chloride reduced fluid transport. Although these in vitro treatments nullified the stimulatory effects of prolactin, only phlorizin and ouabain significantly decreased sodium transport. These results suggest that the effects of prolactin on intestinal transport may be dependent on increased movement of sodium.
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PMID:Further studies on the action of prolactin on fluid and ion absorption by the rat jejunum. 112 80

Prolactin (PRL) responds to several stimuli that elicit release of adrenocorticotropin (ACTH), but does not increase in response to hemorrhage in fetal animals. To determine whether PRL increases after hemorrhage in older animals, 11 immature female swine were prepared chronically under halothane and conditioned behaviorally to lie in a sling. They were bled 14 ml/kg over 5 min. PRL, ACTH, cortisol (F), lysine vasopressin (LVP), and pressure renin activity (PRA) were measured by radioimmunoassay. Epinephrine (EPI) and norepinephrine (NE) were separated by high-performance liquid chromatography. Arterial PRL increased at 0.75 and 1 h (P less than 0.01) and paralleled ACTH and F that peaked at 0.75 h (P less than 0.05 and P less than 0.01, respectively). All three hormones recovered significantly by 4 h. In contrast, PRA and LVP peaked transiently at 0.25 h after hemorrhage and recovered by 1.5 h (P less than 0.05, in each case). EPI and NE did not change significantly. In individual pigs, ACTH and F each showed correlations (Spearman) with PRL that were positive in 10 pigs and significant in six and five pigs, respectively. The pig with the smallest ACTH change (8.4 pg/ml peak) showed no increase in PRL. Peaks in PRL were simultaneous with (five pigs) or delayed by 15 min (four pigs) or 30 min (one pig) from peaks in ACTH. Significant correlations of PRL with PRA and with LVP occurred in only two pigs and in one pig, respectively. A common pathway may contribute to other independent mechanisms controlling the release of ACTH and PRL after hemorrhage.
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PMID:Response of prolactin to hemorrhage is similar to that of adrenocorticotropin in swine. 215 59

In septic patients the clinical course of the disease is characterized by high DIT and rT3 serum concentrations as well as a low T3-syndrome. While rT3 is elevated in almost all critically ill patients, the increase in DIT is indicative of severe infection. Prolactin levels are regularly elevated in sepsis although to variable degrees. Catecholamines and vasopressin should be regarded as acute responders. The pattern of cortisol secretion is uncertain. In most situations the secretion appears to be elevated; the circadian rhythm is disturbed.
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PMID:Patterns of endocrine secretion during sepsis. 255 Sep 59

The secretion of adenohypophyseal hormones is controlled by hypothalamic hypophysotropic hormones with stimulating (hormone releasing factors) or inhibitory (hormone release inhibiting factors) actions. The release of hypothalamic hormones is regulated by hierarchically higher nerve centres via neurons which liberate neurotransmitters at their endings. The secretion of growth hormone is controlled by hypothalamic hormones, somatotropin releasing factor and somatotropin release-inhibiting factor; of the neurotransmitters, the strongest effects have noradrenaline and dopamine. The release of ACTH is controlled by two stimulating hormones, the ACTH releasing factor and vasopressin, the effects of neurotransmitters are less marked, with the involvement of noradrenaline, serotonin, acetylcholine, gamma aminobutyric acid and other agents. Prolactin release is under the main inhibitory control of hypothalamic dopamine, no release-stimulating hypothalamic factor could be unequivocally demonstrated as yet; likely, several peptides are involved in this mechanism. The release of thyrotropic hormone is stimulated by thyrotropin releasing factor, whereas somatotropin release-inhibiting factor has an inhibitory action. Of the neurotransmitters, the inhibitory effect of dopamine is important; this agent however acts also at the hypophyseal level. External hypothalamic hormones and regulatory neurotransmitters are used in the diagnosis and treatment of neuroendocrine disorders.
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PMID:[Central regulation of adenohypophyseal function]. 256 54


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