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- W2012150743 abstract "PGE 2 is a well-known inhibitor of the antidiuretic hormone-induced increase of osmotic water permeability (OWP) in different osmoregulatory epithelia; however, the mechanisms underlying this effect of PGE 2 are not completely understood. Here, we report that, in the frog Rana temporaria urinary bladder, EP 1 -receptor-mediated inhibition of arginine-vasotocin (AVT)-induced OWP by PGE 2 is attributed to increased generation of nitric oxide (NO) in epithelial cells. It was shown that the inhibitory effect of 17-phenyl-trinor-PGE 2 (17-ph-PGE 2 ), an EP 1 agonist, on AVT-induced OWP was significantly reduced in the presence of 7-nitroindazole (7-NI), a neuronal NO synthase (nNOS) inhibitor. NO synthase (NOS) activity in both lysed and intact epithelial cells measured as a rate of conversion of l-[ 3 H]arginine to l-[ 3 H]citrulline was Ca 2+ dependent and inhibited by 7-NI. PGE 2 and 17-ph-PGE 2 , but not M&B-28767 (EP 3 agonist) or butaprost (EP 2 agonist), stimulated NOS activity in epithelial cells. The above effect of PGE 2 was abolished in the presence of SC-19220, an EP 1 antagonist. 7-NI reduced the stimulatory effect of 17-ph-PGE 2 on NOS activity. 17-ph-PGE 2 increased intracellular Ca 2+ concentration and cGMP in epithelial cells. Western blot analysis revealed an nNOS expression in epithelial cells. These results show that the inhibitory effect of PGE 2 on AVT-induced OWP in the frog urinary bladder is based at least partly on EP 1 -receptor-mediated activation of the NO/cGMP pathway, suggesting a novel cross talk between AVT, PGE 2 , and nNOS that may be important in the regulation of water transport." @default.
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- W2012150743 date "2007-07-01" @default.
- W2012150743 modified "2023-10-02" @default.
- W2012150743 title "Prostaglandin E<sub>2</sub> inhibits vasotocin-induced osmotic water permeability in the frog urinary bladder by EP<sub>1</sub>-receptor-mediated activation of NO/cGMP pathway" @default.
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- W2012150743 doi "https://doi.org/10.1152/ajpregu.00811.2006" @default.
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