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)

Blood flow was measured by means of 125I-Antipyrin distribution and was found to be increased in the posterior pituitary of conscious rats following water deprivation for 24 h as compared to either normohydrated control or to force hydrated rats (2.86 ml min-1 g-1 vs. 2.36 ml or 2.08 ml, respectively). Other parameters of systemic haemodynamics, blood flow in the brain or in the hypothalamus and in anterior pituitary did not differ in three experimental groups of rats subjected to various water intake. The increased blood flow in the posterior pituitary in dehydrated rats presumably parallels the locally intensified metabolic rats due to the enchanged stimulation of the antidiuretic hormone release.
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PMID:Water deprivation for 24 hours increases selectively blood flow in posterior pituitary of conscious rats. 30 25

Use of vasopressin injection (Pitressin) as an adjunct in the treatment of various types of gastrointestinal hemorrhage also produces an antidiuretic hormone effect of free water retention. This produces difficulties in fluid and electrolyte management and in the interpretation of changes in mental and hemodynamic status. This effect and its management are directly related to the total dose of the drug administered.
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PMID:Antidiuretic hormone effect of vasopressin therapy for gastrointestinal hemorrhage. 31 81

Unidirectional and net water fluxes were simultaneously estimated in frog urinary bladder. The minute by minute tritiated water (3HOH) transepithelial flux and the net volume of fluid traversing the tissue were employed. It was observed that: (1) the time course of the increase in the 3HOH flux induced by antidiuretic hormone had a very similar pattern to that reported for the increase in the net movement. (2) Unstirred layers strongly affected the magnitude of the antidiuretic hormone-induced increase in 3HOH fluxes while the time course of the response was almost non-affected. In non-stimulated bladders 3HOH fluxes were poorly modified by medium stirring. New steady-state conditions for 3HOH fluxes were established 1 min after stirring rate modifications. (3) The simultaneously determined net water flux was not affected by a modification in the unstirred layers, indicating that the variations in the measured net water fluxes are a good estimation of the changes in the mucosal border permeability. (4) The presence of an osmotic gradient during hormonal challenge (implying net water fluxes, cell swelling and dilation of the intracellular spaces) did not modify the time course of 3HOH movements. These results suggest that the time course of the increase in water permeability is an intrinsic characteristic of the experimental system that could result from the addition of permeability units that increase in number during the development of the hormonal action.
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PMID:Simultaneous minute by minute determination of unidirectional and net water fluxes in frog urinary bladder. A reexamination of the two barriers in series hypothesis. 31 17

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

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

The divalent cation ionophore A 23187 was used to evaluate the action of intracellular calcium on net transepithelial water movement across the isolated frog urinary bladder. Incubation with the ionophore increases the net basal water flux in a dose-dependent fashion but independent of the extracellular calcium concentration. Bladders pretreated with A 23187 and exposed thereafter to an increase in calcium concentration exhibit a water permeability that under certain conditions can be comparable to that achieved with antidiuretic hormone (ADH). Lowering the serosal calcium at the peak of the hydrosmotic responses to both ADH and A 23187 inhibited the maintenance of the net water flux. The action of a supramaximal dose of ADH is blunted in bladders pretreated with A 23187, while the hydrosmotic effects of a submaximal dose are enhanced when the ionophore is added together with the hormone. The results show that an increase in transepithelial water movement can be triggered by calcium and that serosal calcium is needed to sustain the response. This hydrosmotic response may be dependent upon the rate at which intracellular calcium concentrations change and on the absolute concentration attained. It is suggested that calcium is involved in the action of ADH on water permeability and may act as a modulator of the hydrosmotic response.
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PMID:Intracellular calcium as a modulator of transepithelial permeability to water in frog urinary bladder. 34 30

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

An electron microscopic study was made of mouse pituitaries immunocytochemically stained with anti-lysine vasopressin (LVP) as the primary antiserum in the unlabeled antibody peroxidase-anti-peroxidase procedure. Vasopressin (VP) was identified in the neurosecretory granules of the neural lobe which stained with peroxidase anti-peroxidase molecules. Electron density was induced in secretory granules of the pars intermedia (PI), both in the melanocyte stimulated hormone and ACTH cell types, probably indicating VP molecules attached to binding (receptor) sites. Omission of anti-LVP abolished staining both in the neural lobe and the PL Anti-LVP absorbed with antigen, by admixing with LVP, abolished staining in the neural lobe but not in the PI; according to optical density measurements the PI showed a +/- 22% staining increase over controls. Staining intensity in the PI probably reflects occupancy of binding (receptor) sites for VP. Exposure of PI granules to LVP before the usual staining sequence resulted in +/- 48% increased staining. In water-deprived mice with high endogenous VP titers, staining was +/- 33% and +/- 40% more intense than in normal mice. Solid phase absorbed and eluted antibodies to LVP provided additional proof that staining in both neural lobe and PI could be attributed to anti-LVP. Results indicate that binding or receptor sites for VP are located on secretory granules in the PL Possible physiological significance is discussed.
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PMID:Immunocytochemical evidence for vasopressin receptors. 35 43

The authors determined cardiovascular, renal, and hormonal responses to increased airway pressure during continuous positive-pressure ventilation (CPPV) and continuous positive airway pressure (CPAP). Nine healthy, hydrated laboratory swine had appropriate catheters placed to allow for measurement of intrapleural, aortic, inferior vena caval, and left ventricular end-diastolic pressures; cardiac output; and urinary flow. Samples of arterial blood were analyzed for oxygen and carbon dioxide tensions, pH, plasma vasopressin, osmolality, and creatinine and sodium concentrations. Urine was analyzed for osmolality and creatinine and sodium concentrations, and volume was recorded. Intrapleural pressure was subtracted from left ventricular end-diastolic pressure to calculate transmural pressure, a reflection of left ventricular filling pressure. Glomerular filtration rate and urinary free-water and osmolal clearances were also calculated. Expiratory left ventricular filling pressure was decreased equally by CPAP and CPPV. However, inspiratory left ventricular filling pressure and cardiac output were decreased by CPPV only. Urinary flow and glomerular filtration rate were decreased equally by CPAP and CPPV. Sodium excretion was decreased and plasma vasopressin increased by CPPV, but not by CPAP. Urinary free water and osmolal clearances were not changed by either ventilatory pattern. Although many of the renal-function variables were affected similarly by CPPV and CPAP, these alterations were not influenced solely by cardiac output or vasopressin, because only CPPV depressed cardiac output and increased vasopressin levels.
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PMID:Renal function and cardiovascular responses during positive airway pressure. 37 28

Positive end expiratory pressure (PEEP) during respirator therapy can impair renal function by altering renal haemodynamics or by increasing the secretion of the antidiuretic hormone. In the present study, the effect of the commonly used 10 cm H2O PEEP for two hours on renal function and on plasma renin activity was studied in eleven intensive care patients. During the examination period, the patients received analgesic, sedative, and muscle relaxant drugs, but no diuretics. PEEP decreased the mean urinary output by 21%. Urinary specific gravity and osmolality increased. Urinary sodium excretion decreased along with urinary volume. The creatinine clearance decreased slightly, but free water clearance became less negative suggesting reduced ability of tubules to concentrate urine during PEEP. The plasma renin activity was not altered significnalty by PEEP, nor did the urinary sodium/potassium ratio change. This may indicate that the water retention induced by PEEP is not caused by the increased secretion of aldosterone. The results suggest that 10 cm H2O PEEP impairs renal function in critically ill patients and causes mainly water retention.
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PMID:Positive end expiratory pressure ventilation, renal function and renin. 37 92


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