Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin increases the permeability of receptor cells to water and, in tissues such as toad bladder, to solutes such as urea. While cyclic AMP appears to play a major role in mediating the effects of vasopressin, there is evidence that activation of the water permeability system and the urea permeability system involves separate pathways. In the present study, we have shown that inhibitors of oxidative metabolism (rotenone, dinitrophenol, and methylene blue) selectively inhibit either vasopressin-stimulated water flow or vasopressin-stimulated urea transport. There was no inhibition, however, when exogenous cyclic AMP was substituted for vasopressin, and little to no inhibition when the potent analogue 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) was employed. Rotenone had no effect on adenylate cyclase activity or cyclic AMP levels within the cell; dinitrophenol decreased adenylate cyclase activity minimally. Additional studies with vinblastine and nocodazole, inhibitors of microtubule assembly, demonstrated an inhibition of vasopressin and cyclic AMP-stimulated water flow but showed no effect on urea transport. We would conclude that water and urea transport, as examples of hormone-stimulated processes, have different links to cell metabolism, and that in addition to cyclic AMP, a non-nucleotide pathway may be involved in the action of vasopressin.
 ...
PMID:Effect of metabolic inhibitors on vasopressin-stimulated transport systems in the toad bladder. 22 66

The effects of vasopressin and cyclic AMP on water transport at arachnoid villi into the superior sagittal sinus were examined using the isolated meninges preparations of cats. The meninges preparation, the superior sagittal sinus of which was opened at the midline of the outer surface, was held between two polyethylene tubes. The tubes were fixed vertically in the way that the opened surface of the sinus was directed downward and arachnoid surface upward. Water transport was determined by measuring the tritiated water dripping through the membrane preparation. Vasopressin from less than 50 to 500 muU/ml accelerated the water transport and this effect was dose-dependent. Cyclic AMP from 0.5 to 10 mM was proved to manifest the same effect as vasopressin. This effect of cyclic AMP appeared rapidly in comparison with that of vasopressin, suggesting that the effect of vasopressin may be manifested through cyclic AMP. From these findings a physiological role of vasopressin in cerebrospinal fluid was discussed regarding the regulation of intracranial pressure.
 ...
PMID:Effects of vasopressin and cyclic AMP on water transport at arachnoid villi of cats. 22 64

Vsopressin activates a number of transport systems in the toad bladder, including the systems for water, urea, sodium, and other small solutes. Evidence from experiments with selective inhibitors indicates that these transport systems are to a large extent functionally independent. In the present study, we show that the transport systems can be separately activated. Low concentrations of vasopressin (1 mU/ml) activate urea transport with virtually no effect on water transport. This selective effect is due in part to the relatively greater inhibitor action of endogenous prostaglandins on water transport. Low concentrations of 8-bromoadenosine cyclic AMP, on the other hand, activate water, but not urea transport. In additional experiments, we found that varying the ratio of exogenous cyclic AMP to theophylline activated water or urea transport selectively. These studies support the concept of independently controlled systems for water and solute transport, and provide a basis for the study of individual luminal membrane pathways for water and solutes in the accompanying paper.
 ...
PMID:Membrane pathways for water and solutes in the toad bladder: I. Independent activation of water and urea transport. 22 13

Urea and water transport across the toad bladder can be separately activated by low concentrations of vasopressin or 8 Br-cAMP. Employing this method of selective activation, we have determined the reflection coefficient (sigma) of urea and other small molecules under circumstances in which the bladder was transporting urea or water. An osmotic method for the determination of sigma was used, in which the ability of a given solute to retard water efflux from the bladder was compared to that of raffinose (sigma = 1.0) or water (sigma = 0). When urea transport was activated (low concentration of vasopressin), sigma for urea and other solutes was low, (sigma urea, 0.08--0.39; sigma acetamide, 0.55; sigma ethylene glycol, 0.60). When water transport was activated (0.1 mM 8 Br-cAMP) sigma urea approached 1.0 sigma urea also approached 1.0 at high vasopressin concentrations. In a separate series of studies, sigma urea was determined in the presence of 2 x 10(-5) M KMnO4 in the luminal bathing medium. Under these conditions, when urea transport is selectively blocked, sigma urea rose from a value of 0.12 to 0.89. Thus, permanganate appears to "close" the urea transport channel. These findings indicate that the luminal membrane channels for water and solutes differ significantly in their dimensions. The solute channels, limited in number, have relatively large radii. They carry a small fraction (approximately 10%) of total water flow. The water transport channels, on the other hand, have small radii, approximately the size of a water molecule, and exclude solutes as small as urea.
 ...
PMID:Membrane pathways for water and solutes in the toad bladder: II. Reflection coefficients of the water and solute channels. 22 14

The mucosal surface of toad urinary bladder was examined with scanning electron microscopy following its exposure to 20 mU/ml of vasopressin (VP), 10(-4) M 8-bromo-cAMP, 1 mM acetylcholine chloride, serosal hypertonicity, or a hypotonic bathing medium. After a 30-min exposure to VP, the arborizing ridge-like surface pattern typical of granular cells was transformed into microvilli, a response that was not dependent on transepithelial osmotic water movement. An identical response occurred following a 30-min exposure of the bladder to 8-bromo-cAMP, again in the absence of an osmotic gradient. Microvillus formation was not observed when cell volume was increased by incubation of tissue in half-normal amphibian Ringer's solution for 30 min, or with exposure to acetylcholine, which caused accentuation of the convexity of the apical surface of the granular cell similar to that observed with VP-induced osmotic water flow. However, 60 min of incubation in a hypertonic serosal medium (mannitol, 240 mM) caused transformation of ridges to microvilli mimicking the picture obtained with VP. These findings establish that transepithelial osmotic water flow with cell swelling is not required for microvillus formation on the apical surface of granular cells following VP stimulation, and that the surface changes are not due to cell swelling alone or to changes in the configuration of the apical plasmalemma. The results also suggest that the response to VP is mediated via the generation of cAMP. Finally, this study demonstrates that serosal hypertonicity also causes transformation of ridges to microvilli by a mechanism that is yet to be defined.
 ...
PMID:Effect of vasopressin and serosal hypertonicity on toad urinary bladder. 23 89

Aqueous vasopressin was infused to bicarbonate- and glucose-loaded dogs and to nonloaded antidiuretic dogs in doses of 50 mU/kg per min or 50 mU/kg per h. Both doses caused a marked increase in sodium, chloride, and water excretion. The larger dose raised the fractional excretion (sodium clearance (C-Na)/glomerular filtration rate (GFR) times 100) of these ions from 2% or less to in excess of 20%. Blocking the pressor effects of these doses of vasopressin with sodium nitroprusside did not alter the marked natriuretic and chloriuretic effect. The maximal rate of bicarbonate and glucose reabsorption was not depressed by vasopressin infusion; fractional phosphate excretion, however, was markedly increased. Inhibiting distal hydrogen ion secretion by inducing selective aldosterone deficiency failed to uncover a vasopressin-induced inhibition of proximal bicarbonate reabsorption that might have been masked by increased distal bicarbonate reabsorption. There was no significant change in GFR, renal plasma flow, or filtration fraction. The distribution of cortical renal blood flow (measured by the radioactive microsphere technique) shifted toward the inner cortex after vasopressin administration. Vasopressin, in pharmacologic doses, is a potent diuretic that most likely exerts this effect by directly inhibiting sodium reabsorption at a point in the nephron distal to the proximal tubule.
 ...
PMID:Effect of infusion of pharmacologic amounts of vasopressin on renal electrolyte excretion. 23 93

The effects of intravenous infusion of ornithine-vasopressin (OVP) and desamino-D-arginine-vasopressin (dDAVP) were studied in normal and hydrated Merino sheep. In normal sheep, OVP resulted in a diuresis, increased urinary sodium and potassium excretion, and a fall in the plasma potassium concentration. Renal plasma flow remained constant but glomerular filtration rate and filtration fraction rose markedly. dDAVP in normal sheep was antidiuretic, but its only significant effect was a small decrease in plasma osmolality. In the hydrated sheep OVP was antidiuretic and resulted in increased urinary excretion of sodium and potassium, and a fall in the plasma potassium level. Renal plasma flow fell, but glomerular filtration and filtration fraction tended to rise. dDAVP in the hydrated sheep was also antidiuretic but urinary sodium and potassium excretion was reduced. Renal plasma flow and glomerular filtration fell, with a small decrease in filtration fraction. These results suggest that the diuretic effect in normal sheep and the electrolyte-excreting effects in both normal and hydrated sheep of OVP are related to the increase in glomerular filtration, which in turn is dependent on the vasopressor activity of the hormone. The increase in glomerular filtration caused by OVP is due to an increase in the filtration fraction of an unchanged renal plasma flow, which could be brought about by an increase in renal efferent arteriolar tone. The effects of hydration of the sheep were the conventional increased urine flow, decreased urine osmolality and decreased solute-free water reabsorption. Sodium and potassium excretion rose slightly and plasma osmolality fell. Renal plasma flow and glomerular filtration both increased with little change in filtration fraction. These effects could be brought about by suppression of endogenous vasopressin and a decrease in both afferent and efferent renal arteriolar tone.
 ...
PMID:The effects of two analogues of arginine-vasopressin (ornithine-vasopressin and desamino-D-arginine-vasopressin) on kidney function in sheep. 24 35

Conscious Merino ewes were given an intravenous hypertonic sodium chloride load of 4 mmol.min-1 for 100 min. This resulted in increases in urine flow, sodium and potassium excretion and plasma sodium concentration and osmolality. Urinary vasopressin output and solute-free water reabsorption increased and plasma renin activity declined. Renal plasma flow and glomerular filtration rate (GFR) rose, as did the solute clearance. The change in urinary osmolality was related to the initial urine osmolality such that when the initial urine osmolality was high the urine became more dilute, and vice versa. Tubular sodium reabsorption increased but the fractional reabsorption rate fell. It is suggested that the increase in GFR was at least partly due to the increase in AVP and that the electrolyte loss can be accounted for by the increase in GFR without necessarily involving AVP or other hormonal effects at the tubular level.
 ...
PMID:The effect of intravenous hypertonic saline infusion on renal function and vasopressin excretion in sheep. 25 75

Antibovine neurophysin antibodies (anti-bNpI and/or anti-bNpII) are present in certain patients with familial central diabetes insipidus; these are exogenous origin, as they are not present in patients who have not received treatment with crude posterior pituitary extracts over the years preceding the analysis. Immunoreactive neurophysins were detectable in the blood of five patients with familial central diabetes insipidus, and in two of them, the levels increased after a short period of water restriction. There is marked polymorphism of these neurophysins from one serum to another: neurophysin I was consistently absent, while neurophysin II, accessory neurophysins, and other immunoreactive substances not present in normal sera were sometimes present in variable amounts. Immunoreactive AVP was undetectable in the urine of all patients, while immunoreactive OT was found in three of them; the latter substance could, however, be arginine vasotocin. Data are presented suggesting that the association between the biosynthesis of neurophysin I and AVP on the one hand, and neurophysin II and OT on the other hand is maintained in patients with isolated AVP deficiency on the basis of a congenital defect.
 ...
PMID:Serum Neurophysins in familial central diabetes insipidus. 26 36

Seven patients with compensated liver cirrhosis and esophageal varices, all with a base line wedge hepatic vein pressure greater than 20 cm H2O, received 1-mg doses of vasopressin hormonogen (tGLVP) intravenously. There was a significant mean decrease in wedge pressure of 32%, which lasted for at least 20 min (the duration of measurement), with no change in cardiac output measured. The only cardiac response was a 10 to 20% bradycardia at the height of the moderate pressor response-otherwise the ECG was without change. In 5 patients who received the same tGLVP dose during surgery, direct measurements of portal venous pressure showed the same degree of decrease within 10 min of intravenous injection. Fifteen patients with liver cirrhosis and severe bleeding from esophageal varices were treated conservatively with blood transfusion and tGLVP as the only major drug aside from antibiotics. A nonrandomized control group of 13 patients with the same age distribution, stage of disease, number of previous bleeds, etc., was treated conservatively in the same manner, except that they received either no hemodynamically active drugs or short acting neurohypophysial peptide preparations such as Pitressin. In the control group there was a 61.5% total mortality, a 53.8% mortality directly related to uncontrollable bleeding, and a mean duration of the bleeding episode of 11 days. In the tGLVP-treated group total mortality was 20%, mortality directly related to uncontrollable bleeding was 13.3%, and mean duration of the bleeding episode was 2.9 days. These results appear to justify a large scale clinical trial of the vasopressin hormonogen in this disease.
 ...
PMID:Action of the triglycyl hormonogen of vasopressin (glypressin) in patients with liver cirrhosis and bleeding esophageal varices. 30 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>