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)

Activity of the Na pump was judged by Na extrusion in epithelial cells loaded with Na by a previous incubation in K-free solutions in the cold. Oxytocin significantly stimulated Na extrusion either at normal (3.5 mM) or low (0.25 mM) K in the medium. It was stimulated as well by cyclic AMP. Maximal concentrations of either agent caused about the same degree of stimulation. Addition of ouabain or removal of K prevented the action of both agents, but amiloride showed no effect at all. These results strongly suggest that, a) neurohypophyseal hormones not only increase Na entry across the mucosal barrier of the epithelium but they also stimulate the serosal Na pump, b) cyclic AMP not only mediates the action of neurohypophyseal hormones on Na and water permeability of the mucosal barrier, but it also mediates the action of the hormones on the Na pump of the serosal barrier.
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PMID:Sodium pump stimulation by oxytocin and cyclic AMP in the isolated epithelium of the frog skin. 20 19

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

Cardiorespiratory, thermal, and renal responses to a 30-min head-out immersion in 15 degree C water were studied at 1-ATA air and 11-ATA helium-oxygne environments in four male subjects wearing dry suits. Cardiorespiratory responses to immersion (reductions in heart rate, expiratory reserve volume, vital capacity, and thoracic impedance; and increases in stroke volume, cardiac output, and inspiratory capacity) were comparable at both pressures. However, thermal responses to immersion (a reduction in mean skin temperature and increases in skin heat flux and suit conductance) were significantly greater at 11 ATA compared to those at 1 ATA. The rate of urinary excretion of norepinephrine increased significantly during and after immersion at 11 ATA but not at 1 ATA. In contrast, the urinary excretion of epinephrine was not altered by pressure or immersion. The immersion diuresis was greater and lasted longer at 11 ATA than at 1 ATA although there was no difference in the endogenous creatinine excretion . This diuresis was accompanied by a significant natriuresis which was more marked at 1 ATA than at 11 ATA. At 1 ATA, the urinary excretion of both aldosterone and antidiuretic hormone (ADH) decreased during immersion. At 11 ATA, the rate of excretion of these hormones before immersion was lower compared to that at 1 ATA and did not change significantly during immersion. These results indicate that immersion in a hyperbaric helium-oxygen environment presents a greater cold stress than at 1-ATA air, and also that immersion diuresis and natriuresis at high pressure may be induced by a factor other than inhibition of aldosterone and ADH.
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PMID:Physiological responses to head-out immersion in water at 11 ATA. 63 73

Freeze cleaving electron microscopy has shown that fusion of isolated secretory vesicles from bovine neurohypophyses was induced by Ca2+ in micromolar concentrations. Mg2+ and Sr2+ were ineffective. Mg2+ inhibited Ca2+-induced fusion. In suspensions containing secretory vesicles as well as sheets of cell membrane, release of vasopressin parallel to intervesicular fusion and fusion of secretory vesicles with sheets of cell membrane was observed after exposure to Ca2+. Mg2+ and Sr2+ were ineffective in replacing Ca2+ as trigger for fusion or vasopressin release. Intervesicular fusion and exocytotic profiles were observed when isolated neurohypophyses or neurosecretosomes were exposed to cold.
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PMID:Fusion of neurohypophyseal membranes in vitro. 90 83

A sensitive and specific double antibody radioimmunoassay has been developed capable of measuring LH-RH in extracted human plasma. Thyrotropin releasing hormone, lysine vasopressin and most of LH-RH analogues did not appear to affect the assay. Hypothalamic extract and some of the LH-RH analogues produced displacement curves which were parallel to that obtained with the synthetic LH-RH. Sensitivity of the radioimmunoassay was about 3 pg per assay tube. The coefficient of variation of intraassay was 6.4%, while that of interassay was 9.6%. Exogenous LH-RH could be quantitatively extracted by acidic ethanol when varying amounts of synthetic LH-RH were added to plasma. Immunoreactivity of LH-RH was preserved in plasma until 2 hr in the cold and gradually reduced thereafter. The plasma levels in LH-RH were 20 pg/ml or less in normal adults and not detectable in children. The aged males over 60 yr and postmenopausal women showed a tendency to have higher levels of plasma LH-RH. Plasma LH-RH level was significantly higher in midcycle than in follicular and luteal stages. The disappearance rate of LH-RH from the circulation after intravenous injection could be represented as half times of 4-6 min. Between 0.2-0.4% of the injected dose was excreted into urine within 1 hr. These results indicate that the determination of LH-RH might be a useful tool for elucidating hypothalamic-pituitary-gonad interactions.
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PMID:Radioimmunoassay for luteinizing hormone releasing hormone in plasma. 110 Mar 64

Renal clearances and plasma antidiuretic hormone (ADH), 17-hydroxycorticoids, and norepinephrine were measured in unrestrained dogs before and during exposure to ambient cold (minus 4 to + 4 degrees C). Some dogs were treated with an inhibitor of cortisol biosynthesis, Metopirone, either alone or combined with dexamethasone, a potent glucocorticoid suppressing ACTH release. Plasma ADH increased in the Metopirone-treated group (P smaller than 0.02) but changed little in other dogs. Plasma 17-hydroxycorticoids in untreated dogs rose from a control value of 14.4 plus or minus 1.9 (SE) to 1.82 plus or minus 1.2 mug/100 ml after 20 min of exposure (P smaller than 0.01), an increase comparable with that previously observed in restrained dogs. Plasma norepinephrine increased from 0.98 plus or minus 0.07 to 1.15 plus or minus 0.08 mug/liter (P smaller than 0.01) after 20 min of exposure. Urine flow, C-Cr, and C-PAH tended to increase spontaneously in nonexposed control dogs. Exposure to cold abolished or reversed this tendency, most distinctly in the Metopirone-dexamethasone group. The urine concentration, measured as T-c-H2O/C-Cr, did not change in cold, in contrast to a decrease previously observed in restrained dogs. The data do not support the key role of plasma cortisol elevation in the mechanism of urine-concentration defect in cold and demonstrate important differences between responses of restrained and unrestrained animals.
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PMID:Plasma hormone and renal function changes in unrestrained dogs exposed to cold. 111 60

A new hypothesis is presented for the first time to explain the etiology of osteoporosis. Prostaglandins (E2 and F2 alpha) at precise concentrations, have been observed to be involved in bone formation. A close association exists between levels of prostaglandins (E2 and F2 alpha) demonstrated in the neonatal mouse leading to bone formation, with estimated prostaglandins (E2 and F2 alpha) concentrations reported in man. Several hormones (vasopressin, oxytocin, luteinizing hormone, follicle-stimulating hormone, cortisol, estradiol, and testosterone) can indirectly affect prostaglandin formation leading to reduced bone formation. The association between these hormones and prostaglandins (E2 and F2 alpha) explains the physiological mechanism whereby estradiol can be effective for the treatment of osteoporosis. This association also explains the etiology of lumbar spondylitis/spondylodynia, reasons for complaints of increased pain in wet cold weather among arthritics and a multitude of other events. Mechanisms related to this interaction between various hormones and the effect of prostaglandins (E2 and F2 alpha) on bone formation are discussed.
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PMID:New clues into the etiology of osteoporosis: the effects of prostaglandins (E2 and F2 alpha) on bone. 132 11

The effects of a single intraperitoneal injection of ethanol (3 g/kg b.wt.) on the hypothalamic-pituitary-thyroid system was explored as a possible explanation of the hypothermic effect of ethanol. Serum thyroid hormones were significantly reduced by ethanol injection, but ethanol did not affect the cold-induced increase in serum thyroid hormones or thyroid-stimulating hormone (TSH). Since cold-exposure stimulates serum levels of TSH and thyroid hormones by stimulating thyroid-releasing hormone (TRH) release from neurons of the PVN, these findings demonstrate that ethanol did not block pituitary response to TRH or thyroid response to TSH. Paradoxically, ethanol increased cellular levels of TRH mRNA in the paraventricular nucleus (PVN), and blocked the cold-induced increase in TRH mRNA, suggesting that ethanol uncouples the regulation of TRH gene expression from the regulation of TRH release specifically in neurons of the PVN. Measurements of the effects of ethanol on TRH mRNA in thalamus, and beta-actin, vasopressin, somatostatin and corticotropin-releasing hormone (CRH) mRNAs in the PVN in addition to TRH mRNA revealed very specific effects of ethanol on the TRH neuronal system.
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PMID:Ethanol blocks the cold-induced increase in thyrotropin-releasing hormone mRNA in paraventricular nuclei but not the cold-induced increase in thyrotropin. 135 12

The effect of a cold pressor test (CPT) on haemodynamics in relation to general and regional sympathetic activity and arginin vasopressin (AVP), was studied in eleven patients with severe congestive heart failure (CHF). Compared to an age-matched control group (C), resting arterial plasma noradrenaline (NA) (419 +/- 77 vs. 182 +/- 15 pg ml-1), and adrenaline (A) (142 +/- 28 vs 54 +/- 10 pg ml-1) were higher (P less than 0.05) in CHF. AVP showed no significant difference (14 +/- 4 vs. 9 +/- 4 pg ml-1). During CPT systolic and diastolic blood pressure and systemic vascular resistance increased (P less than 0.01), as did NA (delta 114 +/- 39 pg ml-1, P less than 0.01), A (delta 33 +/- 10 pg ml-1, P less than 0.01) and heart rate (delta 10 beats min-1, P less than 0.01). The myocardial v-a difference of NA decreased (P less than 0.05), but was unchanged across the renal vascular bed during CPT. The a-v difference of NA in the hepatic vascular bed, and fractional extraction of A in the coronary sinus, renal and hepatic vascular beds remained unchanged during CPT. AVP did not change significantly and no change in cardiac index or left ventricular filling pressure was observed during CPT. These data suggest that despite an increased activation of the sympathetic nervous system at rest, a further increase in blood pressure and catecholamines took place during CPT. Thus, the effect of a CPT which activates the central sympathetic system seems not to be altered in patients with severe CHF.
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PMID:Haemodynamic and neurohumoral effects of cold pressor test in severe heart failure. 154 Oct 87

Classically, cold induced plasma volume reduction is explained by an increased diuresis which is generated by an inhibition of antidiuretic hormone release. However, most of the haemoconcentration appears to be reversible during rewarming. This observation weakens the former statement. The aim of this study was to clarify the mechanisms involved in the reversal of the cold induced haemoconcentration. Six young males, resting in a dorsal reclining position, were exposed successively to a thermoneutral environment (30 min), a cold environment (1 degrees C; cold) or thermoneutrality (control) for 120 min, and during a 60-min recovery period in thermoneutral conditions. During cold stress, a reduction of 15% (i.e. 510 ml) of the plasma volume was observed, and osmolality was unchanged. After the 60-min recovery under thermoneutral conditions, plasma volume variation between the Cold and the Control experiments was reduced and reached 3% (i.e. 100 ml). This volume equalled the increased amount of urine production observed during the cold stress experiment. Haemoconcentration cannot be explained by increased urinary water loss (+/- 100 ml) alone. Therefore a transient shift of plasma water from vascular to interstitial spaces, due to an increase of blood pressure, could be involved in the reduction of plasma volume.
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PMID:Reversal of cold induced haemoconcentration. 156 70


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