THE POSSIBLE INVOLVEMENT OF ENDOTHELIUM DERIVED HYPERPOLARIZING FACTOR IN MECHANISM OF RELAXATION INDUCED BY CARBACHOL IN RABBIT ISOLATED RENAL ARTERY
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In this study the isolated rabbit renal artery segments contracted with 0.1 μM phenylephrine and in the presence of nitric oxide synthase inhibitor, N-nitro-L- arginine methyl ester (L-NAME), carbachol produced endothelium-dependent relaxations. In the present work, the mechanism underlying this (L- NAME) resistant relaxation was studied. The relaxation was not affected by cyclooxygenase inhibitor indomethacin. In arteries contracted with 30mM K+ L-NAME resistant relaxation induced by carbachol was absent. The Na + -K+ ATPase inhibitor ouabain reduced this relaxation in a concentration dependent manner. In le free media, addition of K+ (5mM) produced significant relaxation of phenylephrine-induced contraction. This relaxations was endothelium-independent and ouabain-sensitive.Neither le channel blocker Tetraethylammonium (TEA) nor the cytochrome p 450 inhibitor miconazole produce any significantly change the maximal response of renal artery to carbachol. In conclusion, in rabbit isolated renal artery, carbachol produced a non-Nitric oxide, non prostacyline 12 dependent relaxation. This relaxation might be mediated by an endothelium-derived hyperpolarizing factor (EDHF). This factor does not appear to be a cytochrome P450 metabolite. The inhibition by ouabain of these relaxations suggests the possible involvement of Na+ - K+ ATPase activation in EDHF responses although other mechanisms cannot be ruled out.