RENAL VASODILATION TO HISTAMINE IN-VITRO - ROLES OF NITRIC-OXIDE, CYCLOOXYGENASE PRODUCTS AND H-2 RECEPTORS

The aim of this study was to evaluate the roles of nitric oxide (NO) a nd prostanoids in vasodilation to histamine in the preconstricted isol ated perfused rat kidney. Kidneys were excised from Hypnorm/Hypnovel-a naesthetised Wistar rats and perfused at constant flow in vitro. Renal perfusion pressure was elevated similarly with methoxamine (3 mu M) o r modified Krebs Henseleit solution containing high KCl (30 mM) and va sodilation to histamine (10, 30 nmol) and papaverine (30, 100 nmol) wa s then examined before and during perfusion with the NO synthase inhib itor, N-G-nitro-L-arginine methyl ester (L-NAME, 0.3 mM) or the cyclo- oxygenase inhibitor, indomethacin (10 mu M). Furthermore, the vasodila tor response to 30 nmol histamine was examined in the presence of the H-2 receptor antagonist, ranitidine (0.1-10 mu M). Vasodilation to his tamine (10, 30 nmol) was found to be unaffected by L-NAME (0.3 mM) or indomethacin (10 mu M), while ranitidine (0.1-10 CIM) antagonised vaso dilation to 30 nmol histamine with an estimated pA(2) of 6.67. Vasodil ation to histamine in the isolated perfused rat kidney is therefore pr obably independent of NO and prostanoids and mediated by H-2 receptors .