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)

Increases in transepithelial solute permeability were elicited in the frog skin with external hypertonic urea, theophylline, and vasopressin (ADH). In external hypertonic urea, which is known to increase the permeability of the extracellular (paracellular) pathway, the unidirectional transepithelial fluxes of Na (passive), K, Cl, and urea increased substantially while preserving a linear relationship to each other. The same linear relationship was also observed for the passive Na and urea fluxes in regular Ringer and under stimulation with ADH or 10 mM theophylline, indicating that their permeation pathway was extracellular. A linear relationship between Cl and urea fluxes could be demonstrated if the skins were separated according to their open circuit potentials; parallel lines were obtained with increasing intercepts on the Cl axis as the open circuit potential decreased. The slopes of the Cl vs. urea lines were not different from that obtained in external hypertonic urea, indicating that this relationship described the extracellular movement of Cl. The intercept on the ordinate was interpreted as the contribution from the transcellular Cl movement. In the presence of 0.5 mM theophylline or 10 mU/ml of ADH, mainly the transcellular movement of Cl increased, whereas 10 mM theophylline caused increases in both transcellular and extracellular Cl fluxes. These and other data were interpreted in terms of a possible intracellular control of the theophylline-induced increase in extracellular fluxes. The changes in passive solute permeability were shown to be independent of active transport. The responses of the active transport system, the transcellular and paracellular pathways to theophylline and ADH could be explained in terms of the different resulting concentrations of cyclic 3'-5'-AMP produced by each of these substances in the tissue.
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PMID:Actions of external hypertonic urea, ADH, and theophylline on transcellular and extracellular solute permeabilities in frog skin. 108 Jul 96

Studies were carried out in the rat to detemine if hypothalamic lesions which caused polydipsia and polyuria had their effect mediated through an alteration of the ability of the neurohypophyseal system to release ADH. Rats with medial preoptic lesions hadincreased water intake while on ad libitum access to water and slightly impaired ability to conserve water following dehydration, but with no impairment of urine-concentrating ability. These were associated with an increase in plasma osmolality both during ad libitum fluid intake and after dehydration. Urinary ADH excretion was at leastas great as in shamoperated controls during ad libitum water intake, but failed to increase during dehydration in spite of a marked increase in plasma osmolality. Pituitary ADH content did not differ from control animals either during ad libitum water intake of after dehydration. Animals with lesions in the lateral preoptic and septal areas did not differ from control animals during ad libitum fluid intake and after dehydration even though lateral preoptic lesions produced polydipsia. In all animals, lesions were remote from the supraoptic nuclei, which showed no histological evidence of damage. It is concluded thatareas of the central nervous system away from the supraoptic nuclei are involved in the regulation of both water intake and ADH release.
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PMID:Polyuria and imparied ADH release following medial preoptic lesioning in the rat. 113 May 32

These experiments were designed to determine whether angiotensin II (AII) could potentiate the increase in plasma vasopressin (ADH) concentration produced by continuous, nonhypotensive hemorrhage in nephrectomized dogs. Infusion of AII (10 ng/kg.min) into a common carotid artery in nonbled dogs did not increase plasma ADH levels, suggesting that increases in carotid arterial plasma AII concentration alone do not stimulate an increase in ADH release. Subsequently, nephrectomized dogs subjected to nonhypotensive hemorrhage (0.44 ml/kg.min) were infused as follows: 0.9% saline intravenously, AII (10 ng/kg.min) intravenously, or AII (10 ng/kg.min) into the carotid. The Plasma ADH concentration increased in all three groups of dogs during hemorrhage. Although the AII-infused dogs demonstrated significant increases in plasma ADH levels earlier during hemorrhage, these changes were small; there were no statistically significant differences in plasma ADH concentrations among the three groups. These results suggest that increases in plasma AII concentration have little or no significant effect on the volume control of ADH release.
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PMID:Vasopressin release during nonhypotensive hemorrhage and angiotensin II infusion. 114 5

Lysine vasopressin did not increase plasma FFAs level in man and in rat Pitressin and lysine vasopressin did not influence adenyl cyclase activity in rat epididymal fat pad, while ornithine vasopressin induced a statistically significant adenyl cyclase increment. These findings suggest that the adipokinetic acticity of ADH which has been correlated only with the amino acid arginine is also correlated with ornithine.
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PMID:Antidiuretic hormone and lipolysis. 114 94

A study was made of the effect of the antiepileptic carbamazepine on the water metabolism in 13 vasopressin-sensitive and 4 ADH-resistant diabetes insipidus patients. It was found that in 12 ADH-sensitive diabetes insipidus cases the drug decreased the urinary output and the free water clearance, and increased the urinary osmolarity. The diuresis did not change in ADH-resistant diabetes insipidus patients. The investigations suggest that carbamazepine exerts an ADH-like effect, and can be applied with good results in the treatment of ADH-sensitive diabetes insipidus.
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PMID:Anitdiuretic effect of carbamazepine in diabetes insipidus. 115 Mar 63

[4-Phenylalanine]oxytocin was prepared from Z-Cys(Bzl)-Tyr(Bzl)-Ile-Phe-Asn-Cys(Bzl)-Pro-Leu-Gly-NG2 (4) by deprotection with Na in NH3 followed by cyclization of the resulting disulfhydryl compound with ICH2CH2I. The protected peptide 4 was prepared from Boc-Asn-Cys(Bzl)-Pro-Leu-Gly-NH2 by the stepwise solution method. Coupling was effected by a modification of the dicyclohexylcarbodiimide-1-hydroxybenzotriazole preactivation method wherein the precipitate of dicyclohexylurea is removed by filtration prior to mixing of the amino and carboxyl components. The analog was found to be an effective inhibitor of the antidiuretic (ADH) response to exogenous arginine-vasopressin. It produced marked diuresis in the anti-ADH assay at approximately the same dose level as does [Leu4]oxytocin but, in contrast to [Leu4]oxytocin, showed natriuretic activity only at relatively high dose levels. In addition, [Phe4]oxytocin exhibited 0.15% of the oxytocic potency of oxytocin, weak antiavian vasodepressor activity (pA2 = 6.93), and no measurable rat pressor activity.
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PMID:(4-Phenylalanine)oxytocin, an inhibitor of the antidiuretic effect of 8-arginine-vasopressin. 115 80

Acute volume expansion was produced in 9 dogs by infusing a lactated Ringer's solution at 1 ml/kg/min in a volume estimated to increase blood volume by 20%. Volume expansion was maintained by replacing urinary fluid losses with equal volumes of the Ringer's solution. Following volume expansion, the effects of a slow, nonhypotensive hemorrhage on plasma antidiuretic hormone concentration (PADH) were determined and compared to a group of 9 normovolemic dogs subjected to the same hemorrhage procedure, in order to determine if volume receptor control of ADH release would adapt to acute increases in blood volume. Ringer's infusion significantly increased blood volume to 95.2 +/- 3.1 ml/kg (mean +/- SE; P less than 0.01) when compared to a mean normovolemic blood volume of 77.6 +/- 3.4 ml/kg. Volume expansion was associated with a significantly lower PADH (3.2 +/- 1.6 muU/ml) than that in normovolemic dogs (5.7 +/- 1.2 muU/ml; p less than 0.05). Significant increases in PADH (P less than 0.05) occurred in both groups of dogs after 20 and 40 minutes of a continuous, nonhypotensive hemorrhage (0.40 to 0.45 mg/kg/min. Hemmorrhage was also associated with significant decrease in effective left atrial pressure in both groups of dogs after 5, 10, 20, and 40 minutes of hemorrhage (P less than 0.01). There were no significant differences between the two groups of dogs nor were there any significant changes during the experiment within each group for mean arterial blood pressure, arterial pulse pressure, plasma osmolality, plasma sodium concentration and plasma potassium concentration. Effective left atrial pressure and PADH were found to be exponentially correlated with blood volume in bothy hypervolemic and normovolemic dogs. Analysis of covariance of these correlations suggested that the hypervolemic dogs exhibited the same exponential changes in PADH and effective left atrial pressure with decreased blood volume as in the normovolemic dogs. It is concluded that acute volume expansion does not alter volume control of plasma ADH concentration.
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PMID:Volume control of plasma antidiuretic hormone concentration following acute blood volume expansion in the anesthetized dog. 119 3

The effect on water metabolism of 1-deamino-8-D-arginine vasopressin and lysine vasopressin have been studied and compared in 20 vasopressin-sensitive and 2 ADH-resistant diabetes insipidus patients. In every case of ADH-sensitive diabetes insipidus, diuresis decreased and the urinary osmolality increased more markedly and for a longer time with the former than with the latter drug. Both drugs were ineffective in patients with ADH-resistant diabetes insipidus. Administration of 1-deamino-8-D-arginine vasopressin did not cause any side effect. It is concluded that 1-deamino-8-D-arginine vasopressin can successfully be employed in the treatment of ADH-sensitive diabetes insipidus.
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PMID:Treatment of diabetes insipidus with 1-deamino-8-d-arginine vasopressin. 123 63

The intrarenal distribution of 51Cr-labelled red cells and 125I-immunoglobulin M (125I-IgM) was studied in water diuretic control rats and in water diuretic rats infused with argenine vasopressin (ADH) 1 muU per minute and gram rat. The IgM volume after 1 min equilibration time was taken to be a measure of plasma volume. Intrarenal haematocrits were calculated from the red cell and plasma volumes and were expressed as fractions of total body haematocrit. Infusion of ADH provoked a rise in urine osmolality from below 200 to values ranging from 800 to 2000 mosm per kg with only insignificant elevation of arterial blood pressure. Calculated red cell volume was significantly increased in all renal zones whereas calculated regional plasma volumes were not significantly changed by ADH. In all renal zones ADH administration thus involved significant increments in haematocrit; the relative increment was most pronounced in the inner medulla. The results give no direct evidence in favour of or against vasoconstrictive effects of ADH in the rat kidney. However, it may be argued that the haematocrit changes are compatible with increased haemodynamic resistance and reduction of blood flow in all renal zones (especially in the medulla) involving decreased linear velocities and less pronounced tendency to axial accumulation of red cells. ADH may increase haemodynamic resistance in two ways, first by acting as a vasoconstrictor and, second, by indirectly increasing blood viscosity in the medulla by increasing tissue osmolality.
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PMID:Effects of antidiuretic hormone on intrarenal red cell and plasma volumes in the water diuretic rat. 123 44

The distribution of labeled microspheres within the renal cortex was used to evaluate the influence of physiological amounts of antidiuretic hormone on intrarenal blood flow distribution in hypophysectomized dogs and in rats with hereditary diabetes insipidus. In both species, intravenous infusions of ADH caused a significant decrease in the ratio of inner to outer cortical blood flow. The change in blood flow distribution observed in the hypophysectomized dog with ADH was primarily a consequence of a decrease in inner cortical blood flow. No consistent changes in outer cortical blood flow were found. Also in the dog, glomerular filtration rates and electrolyte excretion rates (Na and K) increased following ADH. In contrast, ADH infusion into Brattleboro rats caused no change in glomerular filtration or excretion of Na and K.
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PMID:Influence of antidiuretic hormone on intrarenal blood flow distribution in diabetes insipidus dogs and rats. 125 56


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