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)

The effects of indomethacin (INDO) and imidazole (IMID) on postobstructed kidney functions were evaluated in dogs after 24 h of bilateral ureteral obstruction (BUO). In vehicle-treated dogs 1 h after release of BUO, clearances of inulin and PAH (Cin and Cpah) were 37 and 26%, respectively, of the preobstruction values. Fractional sodium excretion (FEna) increased from 0.5 +/- 0.1 to 2.9 +/- 0.6. Urine osmolality (Uosmol) increased by 55 +/- 9 mosmol/kg H2O in response to 50 mU of aqueous vasopressin. In INDO-treated dogs, Cin and Cpah were 39 and 21%, respectively, of the preobstruction values. FEna increased from 0.7 +/- 0.2 to 4.0 +/- 0.9. Uosmol increased by 91 +/- 19 mosmol/kg H2O in response to vasopressin. This lack of beneficial effects of INDO may reflect its cancelling effect on prostaglandins' and thromboxanes' (TX) effects on the renal hemodynamics of the postobstructed kidney. To further assess the roles of TX in the postobstructed kidney, IMID, and inhibitor of TX synthesis, was given before the release of obstruction. In this group of dogs, the Cin of the postobstructed kidney did not differ from the preobstruction value. CC pah was 45% of the preobstruction value, a level significantly higher than in either vehicle- or INDO-treated dogs. FEna wa 1.5 +/- 0.2 before and 3.5 +/- 2.3 after obstruction. Uosmol increased by 187 +/- 51 mosmol/kg H2O after vasopressin, a level significantly higher than in vehicle-treated dogs. The present study suggests that IMID improves Cin, Cpah, FEna, and concentrating ability of the postobstructed kidney. TX may be responsible for the persistent reductions of Cin and Cpah in the postobstructed kidney.
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PMID:Effect of imidazole on the recovery from bilateral ureteral obstruction in dogs. 714 23

cAMP and Ca2+ acted together with the acute phase cytokine interleukin-1beta (IL-1beta) to inhibit hepatocyte DNA replication. At sub-basal activity of cAMP-dependent protein kinase (PKA), neither IL-1beta nor the Ca2+-elevating hormone vasopressin affected hepatocyte proliferation. Basal level of PKA activity permitted IL-1beta action. Increased PKA activity also permitted vasopressin action and sensitized further towards IL-1beta, which acted at 10-50 pM concentrations. Vasopressin acted via Ca2+/calmodulin-dependent protein kinase II (CaMKII), and its action was mimicked by the serine/threonine phosphatase inhibitor microcystin, which activates CaMKII. Inhibitors (KN93 and KT5926) of CaMKII selectively counteracted the effects of vasopressin and microcystin on hepatocyte proliferation at concentrations similar to those required to inhibit CaMKII in vitro. Two-dimensional gel electrophoresis of 32P-prelabeled hepatocytes revealed a common set of proteins phosphorylated in response to vasopressin and microcystin. Their phosphorylation was counteracted by CaMKII inhibitor (KT5926). Phosphorylation of the CaMKII substrate phenylalanine hydroxylase (PAH; EC 1.14.16.1) was used as an endogenous marker of CaMKII activation. It was found that treatment of the cells with vasopressin or microcystin increased the phosphorylation of PAH, and that the vasopressin-induced PAH phosphorylation was inhibited by KT5926. In conclusion, the Ca2+-elevating hormone vasopressin potentiated the antiproliferative effects of cAMP and IL-1beta through CaMKII activation.
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PMID:Synergistic antiproliferative actions of cyclic adenosine 3',5'-monophosphate, interleukin-1beta, and activators of Ca2+/calmodulin-dependent protein kinase in primary hepatocytes. 932 53

A reversed diurnal excretory rhythm of water, creatinine and electrolytes was observed in a woman with fluid retention that first appeared following a head injury 21 years previously. Synthetic oxytocin injections were given on the premise that she had a selective deficiency of oxytocin with normal vasopressin production. This treatment produced a diuresis and restored a normal excretory rhythm of water, creatinine and electrolytes. Inulin and PAH clearance studies showed that oxytocin increased the daytime glomerular filtration rate. These results suggest the possibility that oxytocin has an additional non-obstetrical physiologic function, viz. the regulation of the normal diurnal rhythm of glomerular filtration rate.
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PMID:Diuretic effect of oxytocin in a patient with reversed diurnal rhythm of water and electrolyte excretion. 1389 Nov 57


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