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)

A slight optokinetic stimulation induces a significant increase of serum levels of antidiuretic hormone 1,1 +/- 0.8 pg/ml (mean +/- SD) to 3,3 +/- 1,9 pg/ml (mean +/- SD). Serum levels of gGH and cortisol remain unchanged, whereas serum prolactin levels decrease slightly. The ADH secretion seems to be the most sensitive hormonal parameter of the stimulation of the vestibular nuclei induced either by the optokinetic stimulation or by the Coriolis effect.
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PMID:[Pituitary hormone secretion induced by optokinetic stimulation (author's transl)]. 68 96

A variety of effects of alcohol on endocrine function are now well documented. Clinically, the most important of these are alcohol-induced 'pseudo-Cushing's syndrome' and a syndrome of hypothalamic-pituitary-adrenocortical unresponsiveness, both of which result from long-term over-indulgence, and impairment of testosterone secretion which may occur following relatively short-term drinking. Evidence indicates that a number of different mechanisms are responsible for mediating the effects of alcohol on endocrine function. In a few instances (e.g. inhibition of vasopressin secretion and impairment of steroidogenesis resulting in a fall in testosterone production rate), alcohol appears to influence directly the release or synthesis of individual hormones. However, the majority of the endocrine effects of alcohol are probably indirect, resulting from either the stress of intoxication (stimulation of cortisol, catecholamines and possibly GH and prolactin), changes in the level of intermediary metabolites (e.g. a fall in circulating FFA stimulating GH secretion) or changes in the metabolism of hormones (e.g. catecholamines, oestrogens, androgens) resulting from alteration in intracellular redox state or tissue damage.
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PMID:Endocrine effects of alcohol. 68 83

In order to know the pituitary reserves of ACTH, GH, LH, FSH, TSH and prolactin in patients with Cushing's syndrome, the responses of these hormones to hydrocortisone, lysine-8 vasopressin (LVP), insulin-induced hypoglycemia, luteinizing hormon-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) were examined before and after treatment. Fourteen patients with Cushing's disease (adrenal hyperplasia), 3 patientswith adrenal adenoma and one patient with adrenal carcinoma were investigated. Before treatment, sufficient response of plasma ACTH to LVP was observed in patients with Cushing's disease, while no response was observed in 3 patients with adrenal adenoma. There was no significant difference in the responses of other pituitary hormones between the patients with Cushing's disease. and the patients with adrenal adenoma. The response of plasma GH to insulin-induced hypoglycemia was impaired in most these patients. The response of plasma TSH to TRH was impaired in 6 of 8 patients tested. The response of plasma LH and FSH to LH-RH were preserved in 6 and 5 of 8 patients, respectively. The response of plasma prolactin to TRH was normal in most patients tested. After treatment, the improvements of the impaired responses of GH, TSH, LH and FSH wereobserved. Therefore, the impaired reserve observed in these patients before treatment seemed to be due to the hypercortisolemia. If the difference of the suppressibility of these pituitary hormones by cortisol may be judged simply from our observation, the orderof the suppressibility is supposed to be ACTH, GH, TSH, LH and FSH, and then prolactin.
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PMID:The pituitary ACTH, GH, LH, FSH, TSH and prolactin reserves in patients with Cushing's syndrome. 80 44

The prolactin (PRL)-releasing activity of porcine stalk median eminence (pSME) was characterized by an in vivo bioassay and concomitant radioi-munoassay of plasma PRL and thyrotropin (TSH) levels. Methanol extracts of pSME stimulated PRL release in 3-day estrogen-primed rats when administered by the intracarotid route in doses ranging from 0.1 to 2.0 pSME equivalents. Synthetic thyrotropin-releasing hormone (TRH) stimulated the release of PRL and TSH in the dose range of 10 to 300 ng. PRL release was greater in response to a maximally effective dose of pSME than the release elicited by a maximal dose of TRH, and pSME administered together with a greater than mazimally effective dose of TRH caused additional PRL but not TSH secretion. Lysine vasopressin and prostaglandin E1 and E2 stimulated PRL release only at doses several orders of magnitude greater than the dose present in pSME. Somatostatin inhibited the release of TSH but not that of PRL whether the stimulus employed was pSME or TRH. The effective inhibitory dose of somatostatin was also significantly greater than the reported hypothalamic content. When pSME was subjected to incubation with plasma, a treatment reported to inactivate TRH, TSH-releasing activity was destroyed to a greater extent than was PRL-releasing activity. When pSME was adsorbed onto charcoal, the supernatant solution was devoid of TRH, as determined by complete removal of a [3H]TRH marker, yet substantial PRL-releasing activity was retained. TSH-releasing activity eluted from the charcoal with methanol was considerably greater than that expected on the basis of the recovery of [3H]TRH, suggesting the presence in the crude extract of a TSH-release inhibitor or of a TSH-releasing factor other than TRH. Based on the above evidence, we conclude that crude pSME contains PRL-releasing substance(s) distinct from the tripeptide TRH.
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PMID:Dissociation of prolactin-releasing activity from thyrotropin-releasing hormone in porcine stalk median eminence. 81 52

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

An osmoregulatory role for prolactin (PRL) in man has been postulated, and PRL secretion has been reported to be influenced by osmotic stimuli. Clinical observation, however, does not support this notion. The effects of water loading, hypertonic saline infusion and nicotine on serum PRL and on renal water metabolism were investigated in 6 normal subjects and in 8 patients with chronic hyperprolactinemia (four with and four without demonstrable pituitary tumors). None of the patients had thyroid, adrenal or vasopressin deficiency. Renal walter handling in these patients was indistinguishable from normal. Likewise, serum PRL was not affected by the stimuli employed in either the normal subjects or the patients. No correlation between degree or duration of hyperprolactinemia and renal water metabolism was found. It is concluded that PRL is not an important osmoregulatory hormone in man.
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PMID:The effect of osmotic stimuli on prolactin secretion and renal water excretion in normal man and in chronic hyperprolactinemia. 83 59

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

Comprehensive studies on body fluid balance on 5 divers were conducted during the Hana Kai II dive (17 days at 18.6 ATA and 7 days of decompression). Daily urine flow increased from about 2000 ml at 1 ATA to 2600 ml at 18.6 ATA, at 31 degrees C. This diuresis was accompanied by a reduction in urine osmolality (from 650 to 500 mOsm) and a slight increase in osmolal clearance. Endogenous creatinine clearance remained at about 173 ml/min throughout the dive. Despite such a sustained diuresis, neither daily water intake nor total body water volume changed significantly. The plasma renin activity changed little, while both plasma aldosterone concentration and urinary aldosterone excretion increased significantly during the first week at 18.6 ATA. The plasma prolactin concentration showed a significant decrease during the first 3 days at 18.6 ATA. The daily excretion of antidiuretic hormone (ADH) decreased significantly (by 40%) 4 days after compression and remained low throughout the rest of the dive. Insensible waterloss at 18.6 ATA was 35% lower than that at 1 ATA. It is suggested that the observed hyperbaric diuresis is due primarily to suppression of ADH as a result of suppression of insensible water loss.
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PMID:Hana kai ii: a 17-day dry saturation dive at 18.6 ATA. III. Body fluid balance. 91 Mar 16


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