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)

1. The diffusional permeabilities of collecting duct membranes to THO, 14C-urea and 22Na+ have been measured at different concentrations of urea, NaCl and mannitol. 2. In the absence of urea in perfusate and bath or in its presence in low concentrations, the diffusional permeability to urea was 2.0 (s.e.m. = 0.15, n = 58) micrometer s-1, compared with 0.87 (s.e.m. = 0.06, n = 29) microgram s-1 when 200 mmol/l urea was present. The permeability of the collecting ducts to THO or Na+ was not affected by the different urea concentrations. 3. High concentrations of sodium chloride increased the diffusional permeability of collecting ducts to water and urea but did not affect the diffusional permeability of the collecting duct to Na+. 4. Mannitol had effects similar to those of sodium chloride. 5. In all media tested there was an increase in THO and urea permeability when supramaximal amounts of antidiuretic hormone were added. The increases in the various media for each substance were similar, despite widely different starting permeabilities. 6. The results suggest that solutes and water move across collecting duct epithelium by several pathways that respond differently to various stimuli.
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PMID:The effects of sodium chloride, urea and mannitol on the permeability in vitro fo rat papillary collecting ducts to THO, 14C-urea and 22Na. 58 72

1. The effects of synthetic rat atrial natriuretic peptides (ANP) on diffusional 22Na+, 36Cl- and tritiated water (THO) permeability of in vitro microperfused rat papillary collecting ducts and the effect in vivo of ANP on stop-flow sodium concentrations in the terminal segment of rabbit nephrons were studied. 2. The addition of 4 x 10(-8) or 4 x 10(-7) mol/l ANP to the medium or perfusion solution did not alter diffusional 22Na+ or 36Cl- permeability of microperfused rat papillary collecting ducts. 3. The basal diffusional THO permeability of papillary collecting ducts was not altered when 4 x 10(-7) mol/l ANP was present in the medium and did not inhibit the increment in diffusional THO permeability induced by vasopressin or reduce the permeability to water in a duct previously stimulated by vasopressin. 4. The administration of ANP (2 micrograms/kg bodyweight) to rabbits in water diuresis did not alter systemic blood pressure but induced a marked natriuresis and increases in urine flow and potassium excretion. This natriuresis was not associated with alterations in stop-flow sodium reabsorptive capacity or sodium permeability of the collecting tubules and ducts. 5. Previously reported in vivo clearance data suggest that ANP causes, at least in part, a natriuresis by altering sodium transport in the medullary collecting ducts. In this study, however, a direct effect could not be demonstrated and it is possible that the medulla needs to be functioning in its normal environment for such effects to be demonstrated.
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PMID:Effect of atrial peptide on collecting duct function. 297 27

The collecting ducts in papillae taken from normal rats have a measurable increase in diffusional tritiated water (THO) permeability with ADH 5 mu unit/ml and this increase is maximal with antidiuretic hormone (ADH) 100 mu unit/ml added to media. The presence of plasma from rats pretreated with lithium to make them polyuric inhibited the response to ADH. The lowest concentration of ADH that caused a measurable increase in diffusional water permeability was 50 mu unit/ml and the increase was maximal with ADH 2000 mu unit/ml. The maximum response to ADH did not differ whether plasma from control or lithium pretreated rats was used. However, the dose-response curve to ADH was shifted to the right by the plasma from lithium-pretreated rats. Lithium added to the plasma from control rats did not alter the response to ADH. It is proposed that lithium given to rats causes a circulatory factor to be produced that inhibits in a competitive fashion the response of the collecting duct to ADH. Such an effect would explain many features of the impairment of water excretion associated with lithium use.
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PMID:The mechanism of polyuria in rats pretreated with lithium studies by in vitro microperfusion. 687 33

An attempt has been made to assess the validity of applying the frictional and viscous coefficients of bulk water to the movement of water and solutes through the urinary bladder of the toad. The temperature dependence of diffusion of THO, C(14)-urea, C(14)-thiourea, and net water transfer across the bladder was determined in the presence and absence of vasopressin. The activation energy for diffusion of THO was 9.8 kcal per mole in the absence of vasopressin and 4.1 kcal per mole with the hormone present. Activation energies simultaneously determined following vasopressin for diffusion and net transfers of water were similar, and in the same range as known activation energies for diffusion and viscous flow in water. Urea had activation energies for diffusion of 4.1 and 3.9 kcal per mole in the absence and presence of vasopressin, respectively. Thiourea had a high activation energy for diffusion of 6.3 kcal per mole, which was unchanged, 6.6 kcal per mole, following hormone. These findings suggest that in its rate-limiting permeability barrier, water is present in a structured state, offering a high resistance to penetration by water. Vasopressin enlarges the aqueous channels so that the core of water they contain possesses the physical properties of ordinary bulk water. Urea penetrates the tissue via these aqueous channels while thiourea is limited by some other permeability barrier.
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PMID:The state of water in the isolated toad bladder in the presence and absence of vasopressin. 1390 90