Nitric Oxide Mediates Cat Hindlimb Cholinergic Vasodilation Induced by Stimulation of Posterior Hypothalamus

Abstract

The aim of this work was to examine whether endotheliumderived relaxing factor (nitric oxide) mediates cat hindlimb cholinergic vasodilation induced by stimulation of the posterior hypothalamus and β-adrenergic vasodilation by I.V. injection of isoproterenol using an inhibitor of nitric oxide synthesis, NW-nitro-L-arginine methyl ester (L-NAME). Without L-NAME, femoral blood flow velocity (FBV) increased during hypothalamic stimulation by 11.2±2.2 cmis (meant SEM) from the baseline value of 8.4±2.2 cm/s and femoral conductance (FC) increased by 0.084±0.021 cmíssimmHg from 0.062±0.016 cmi simmHg, 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 beatsmin). When isoproterenol (1-2 tug I.v.) was injected, FBW and FC increased 5.1±0.56cm/s and 0.048±0.005 cmisimmHg. With L-NAME (20-100 mg I.A.), the rises in AP and HR during hypothalamic stimulation were unchanged but the increases in FBW and FC were significantly blunted to 5.2±3.7 cm/s and 0.0260±0.021 cm/s/mmHg. In contrast, L-NAME did not affect the responses in FBW and FC during stimulation of β-adrenergic receptors. The effect of N'-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 β-adrenergic vasodilation. © 1993, PHYSIOLOGICAL SOCIETY OF JAPAN. All rights reserved.