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)

Single-unit neural activity in the lamina terminalis, a region implicated in osmoregulation, was studied in alpha-chloralose-anesthetized sheep during mild hyperosmotic stimulation (intracarotid infusions of 1.65 M NaCl, 3 M sorbitol in 0.15 M NaCl, or 3 M urea in 0.15 M NaCl, at 1 ml/min). Twelve of 121 units (9.9%) were activated significantly (by 82 +/- 52%) by 2- to 3-min infusions of 1.65 M NaCl. Eleven of these and one untested unit were excited by hypertonic sorbitol (91 +/- 40% increase). Of five units further tested with urea, two were excited (by 19 and 58%). Isotonic or hypotonic NaCl infusions were without effect (eight osmoresponsive units tested). All responsive units were in the median preoptic nucleus (MnPO; nucleus medianus). MnPO units were compared with neurohypophysial fibers (multiunit recordings). Osmotic response profiles were similar; both MnPO units and neurohypophysial fibers responded equally to hypertonic NaCl and sorbitol but less to equiosmolal urea. Both MnPO units and neurohypophysial fibers responded slowly, taking 50 and 30 s of NaCl infusion, respectively, to show significant increases and approximately 2 min to reach peak activity. Their hemodynamic responses differed, however; neurohypophysial fibers were strongly excited by nitroprusside-induced hypotension (three of three animals) but MnPO osmoresponsive units were not (zero of five units). Osmoresponsive MnPO units may contribute osmotic, but not hemodynamic, inputs to control vasopressin secretion and/or osmoregulatory responses.
 ...
PMID:Osmoresponsive units in sheep median preoptic nucleus. 239 17

Maximal doses of vasopressin increase the permeability of the skins of Bufo bufo and Rana esculenta to urea, ethylene glycol, glycerol, erythritol, beta-alanine, leaving virtually unmodified that of mannitol and antipyrine. These results demonstrate that the response to vasopressin is quite different in amphibian skins as compared to the bladders. A careful analysis of the effects of vasopressin on non-electrolyte permeability as a function of their molecular weight demonstrates that hormone elicits the formation of pores with a diameter inferior to 4 A. Under vasopressin treatment the skins exhibit a selectivity for polyhydroxylated molecules as compared to urea and beta-alanine. This selectivity is not due to active of facilitated transport and is not impaired by phloretin or DTNB which selectively blocks the permeability of urea or ethylene glycol in erythrocytes. It is proposed that the site of such selectivity is located in other plasma membranes of the epithelium.
 ...
PMID:Effect of vasopressin on the permeability of non electrolytes across the skins of Rana esculenta and Bufo bufo. 241 8

Using rat renal papillary collecting tubule (RPCT) cells in culture, we examined the interactions of extracellular osmolality, vasopressin-stimulated cAMP, and prostaglandin E2 (PGE2) synthesis. Hypertonic solutions composed of equiosmolar amounts of urea and sodium chloride, 900-2,400 mosM, potentiated the increases of intracellular cAMP after vasopressin stimulation. Sodium chloride, rather than urea, was the important solute. The mechanism of this augmented cAMP response was complex, probably involving increased synthesis, decreased degradation, and reduced efflux of cAMP from the RPCT cells. The potentiating actions of hypertonic sodium chloride were specific for vasopressin-stimulated cAMP and were not observed for forskolin or PGE2-stimulated cAMP. Hypertonic solutions inhibited RPCT cell PGE2 production, and sodium chloride, rather than urea, was again the important solute. The enzymatic site of sodium chloride inhibition of PGE2 synthesis was apparently on the phospholipase enzymes, assessed by calcium ionophore and bradykinin stimulation, and not on cyclooxygenase, measured by arachidonic acid responsiveness. Reductions of osmolality, from 1,800 to 300 mosM, acutely increased PGE2 release, possibly through a calcium-dependent stimulation of phospholipase. We conclude that conditions that prevail in vivo during antidiuresis, namely hypertonicity of the papillary interstitium, may augment vasopressin responsiveness through increments of collecting tubule cAMP and reductions of PGE2 which could, in concert, maximize water reabsorption in the collecting tubule.
 ...
PMID:Osmolality, vasopressin-stimulated cAMP, and PGE2 synthesis in rat collecting tubule cells. 242 57

Vasopressin is the primary physiological factor regulating renal water reabsorption in mammals. Inhibitors of vasopressin-stimulated water reabsorption have previously been used as water diuretic agents in both experimental animals and man. The present studies describe and characterize the pharmacological effects of the potent vasopressin antagonist desGly d(CH2)5D-Tyr(Et)VAVP (SK&F 101926) and related analogs on renal water and solute excretion in conscious rats. Administration of SK&F 101926 was associated with dose-dependent increases in renal water excretion in conscious hydropenic rats. A selective vasopressin pressor (V1) antagonist (SK&F 100273) was inactive as a diuretic agent in these tests. SK&F 101926 antagonized, in a competitive fashion, exogenous vasopressin-stimulated antidiuresis in conscious water-loaded rats. Only modest increases in renal excretion of Na+, K+, and urea were observed when SK&F 101926 was administered. No changes in endogenous creatinine excretion were associated with the administration of SK&F 101926, suggesting that this drug does not affect glomerular filtration rate. The rank order of bioequivalency of alternative routes of administration of SK&F 101926 was intraperitoneal = intravenous = intramuscular = subcutaneous greater than intranasal much greater than rectal, ocular, and oral. SK&F 101926 (20 micrograms/kg/day) was effective in blocking the development of hyponatremia in a rat model of the syndrome of inappropriate antidiuretic hormone (SIADH). SK&F 100273 (100 micrograms/kg) hastened the onset of endotoxin-associated shock in rats. We conclude that SK&F 101926 is a potent water diuretic (aquaretic) agent in rats. The mechanism of action is most probably antagonism of vasopressin at renal epithelial (V2) receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Discovery and therapeutic utility of vasopressin antagonists in rats. 243 70

The role of vasopressin in the kidney has classically been considered to result from its ability to increase water permeability in the collecting duct. Recent data, however, suggest that the hormone may also promote urinary concentration by increasing interstitial tonicity. The mechanisms whereby vasopressin could enhance interstitial tonicity include increasing urea permeability in the inner medullary collecting tubule, stimulation of solute reabsorption in the thick ascending limb of the loop of Henle, increasing the glomerular filtration rate of juxtamedullary nephrons, and decreasing vasa recta blood flow. We review experiments directed at assessing the role of vasopressin in these four processes. The multitude of effects of vasopressin appears to be well integrated and contributes to the tightly regulated urinary concentration mechanisms.
 ...
PMID:Vasopressin and the concentrating mechanism. 243 73

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.
 ...
PMID:Vasopressin in hyponatremia: what stimuli? 243 81

Forskolin, a natural diterpene activating the adenyl cyclase in a receptor-independent manner, increases symmetrically both transepithelial fluxes of urea and erithrytol through the frog skin. The effect is dose-dependent, being 5 X 10(-6) M the dose necessary to obtain the maximal action. Forskolin-induced permeabilization is inversely proportional to the molecular weight of water soluble molecules (urea greater than erythritol greater than mannitol); also the permeability of a mainly lipid soluble molecule, i.e. antipyrine, is slightly increased by the diterpene. The permeability pattern is more similar to that induced by isoprenaline as compared to that elicited by vasopressin. Differently from what occurs in other tissues, small doses of forskolin (10(-8) M) are unable to potentiate the actions of vasopressin and isoprenaline on urea permeability across the frog skin. Moreover, the maximal action of forskolin is not additive with the maximal ones of isoprenaline and vasopressin.
 ...
PMID:Action of forskolin on non-electrolyte permeability across the frog skin as compared to that of vasopressin and isoprenaline. 244 77

Vasopressin stimulates the introduction of aggregated particles, which may represent pathways for water flow, into the luminal membrane of toad urinary bladder. It is not known whether water transport pathways are degraded on removal from membrane or whether they are recycled. We examined the effect of the protein synthesis inhibitors cycloheximide and puromycin using repeated 30-min cycles of vasopressin followed by washout of vasopressin, all in the presence of an osmotic gradient, a protocol that maximizes aggregate turnover. "High dose" cycloheximide (200 micrograms/ml) inhibited flow immediately. "Low dose" cycloheximide (1 microgram/ml) did not affect initial flow; however, flow was inhibited by the fourth restimulation. On further rechallenge, inhibition persisted but did not increase. In the absence of vasopressin, inhibition did not develop. Despite the inhibition of flow in vasopressin-treated tissues, the cAMP-dependent protein kinase ratio (-cAMP/+cAMP), an index of in vivo cAMP effect, was elevated in cycloheximide-treated tissues, suggesting modulation at a distal site in the stimulatory cascade. Cycloheximide inhibited flow when 10 microM forskolin or 0.2 mM 8-BrcAMP was substituted for vasopressin in the fourth period; however, MIX (4 mM)-stimulated flow was enhanced by 1 microgram/ml cycloheximide but inhibited by 200 micrograms/ml cycloheximide. [14C]urea permeability was not inhibited by cycloheximide. Puromycin (0.5 mM) also inhibited water flow by the fourth challenge with vasopressin. The data suggest that protein synthesis inhibitors attenuate flow at a site that is distal to cAMP-dependent protein kinase.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Protein synthesis inhibitors attenuate water flow in vasopressin-stimulated toad urinary bladder. 244 2

1--The mechanism of the vasopressin-induced, facilitated transport across toad urinary bladder was studied by treating the luminal membrane of the epithelium with the following reagents of protein functional groups: NEM (SH groups), SITS (amino groups), EEDQ (carboxylic groups), DEPC (histidine). 2--Treatment of the luminal side of the epithelium by NEM strongly inhibits the ADH-induced urea transport, leaving unmodified the effect of the hormone on the flux of antipyrine, a lipid soluble molecule. These results confirm the hypothesis that the urea carrier is of proteic nature. 3--Treatment of the luminal side by SITS strongly inhibits ADH action on urea and antipyrine permeability; thus this effect can be considered rather unspecific. 4--On the contrary the EEDQ effect is more specific; in fact treatment of the luminal side by EEDQ strongly inhibits ADH effect on the permeability of urea, slightly increasing the ADH effect on that of antipyrine. 5--Finally, the luminal treatment by diethylpyrocarbonate inhibits almost completely the ADH action on the urea fluxes, slightly increasing the hormone effect on the antipyrine ones. 6--Based on these results we conclude that carboxylic groups and the imidazolic ring are more important than the amino groups in determining the urea transport across toad bladder, in the presence of ADH.
 ...
PMID:Effect of reagents of protein functional groups on the ADH-induced urea facilitated transport across toad urinary bladder. 245 74

Mercurial reagents inhibit the water permeability of erythrocytes and proximal renal tubule. We examined the effect of two such agents on vasopressin-induced water transport across toad urinary bladder. Water flows were measured in unfixed tissues and in tissues fixed either with N-ethylmaleimide (NEM) or with glutaraldehyde. When added concurrently with 20 mU/ml vasopressin, 1 mM mucosal p-chloromercuribenzene-sulfonic acid (p-CMBS) inhibited water flow within 1 h. p-CMBS also inhibited flow in tissues that had been fixed with mucosal NEM after stimulation with vasopressin. However, p-CMBS did not affect flow in glutaraldehyde-fixed tissues. In contrast, HgCl2 inhibited water flow and urea permeability even in tissues that had been fixed with glutaraldehyde after stimulation with vasopressin. Inhibition was more pronounced when HgCl2 was added to the mucosal rather than the serosal bathing medium and was not reversed by dithiothreitol. HgCl2 did not diminish the frequency or area of luminal membrane aggregates observed by freeze-fracture electron microscopy. HgCl2 also did not affect amphotericin-induced water permeability in glutaraldehyde-treated tissues, suggesting that it did not diminish the permeability of cellular barriers to flow. Our results parallel closely those reported by other investigators for water flow across erythrocytes and proximal renal tubule and suggest that mercurial reagents can directly block the vasopressin-induced water channel. The water channel at the apical membrane of the toad bladder may prove to share structural similarity with that constantly present in erythrocytes and proximal renal tubule.
 ...
PMID:Mercurial reagents inhibit flow through ADH-induced water channels in toad bladder. 247 Feb 62


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