NITRIC-OXIDE MEDIATES CAT HINDLIMB CHOLINERGIC VASODILATION INDUCED BY STIMULATION OF POSTERIOR HYPOTHALAMUS

The aim of this work was to examine whether endothelium-derived relaxing factor (nitric oxide) mediates cat hindlimb cholinergic vasodilation induced by stimulation of the posterior hypothalamus and beta-adrenergic vasodilation by I.V. injection of isoproterenol using an inhibitor of nitric oxide synthesis, N(W)-nitro-L-arginine methyl ester (L-NAME). Without L-NAME, femoral blood flow velocity (FBV) increased during hypothalamic stimulation by 11.2+/-2.2 cm/s (mean+/-SEM) from the baseline value of 8.4+/-2.2 cm/s and femoral conductance (FC) increased by 0.084+/-0.021 cm/s/mmHg from 0.062+/-0.016 cm/s/mmHg, which were abolished by atropine (0.5 mg I.A.). Arterial blood pressure (AP) and heart rate (HR) increased during hypothalamic stimulation (15+/-8 mmHg and 22+/-6 beats/min). When isoproterenol (1-2mug i.v.) was injected, FBV and FC increased 5.1+/-0.56 cm/s and 0.048+/-0.005 cm/s/mmHg. With L-NAME (20-100 mg I.A.), the rises in AP and HR during hypothalamic stimulation were unchanged but the increases in FBV and FC were significantly blunted to 5.2+/-3.7 cm/s and 0.026+/-0.021 cm/s/mmHg. In contrast, L-NAME did not affect the responses in FBV and FC during stimulation of beta-adrenergic receptors. The effect of N(G)-monomethyl-L-arginine (10-30 mg I.A.) was the same as L-NAME. It is suggested that nitric oxide is involved in hindlimb cholinergic vasodilation neurally induced by hypothalamic stimulation but not in beta-adrenergic vasodilation.