Forelimb vasodilatation induced by hypothalamic stimulation is greatly mediated with nitric oxide in anesthetized...

The aim of this study was to examine whether or not stimulation of the hypothalamic defense area is capable of inducing sympathetic vasodilatation of the forelimb vascular bed in anesthetized cats. When the hypothalamic defense area was electrically stimulated, brachial blood flow velocity (brachial BFV) and vascular conductance were increased as well as femoral BFV and vascular conductance. Brachial BFV and vascular conductance increased by 110-139% during hypothalamic stimulation. These increases were blunted to approximately one-fifth of the control responses following i.v. injection of a synthesis inhibitor of nitric oxide, N(omega)-nitro-L-arginine methyl ester (L-NAME). The attenuating effect of L-NAME on forelimb vasodilatation evoked by hypothalamic stimulation was greater than that on hindlimb vasodilatation. The combined administration of L-NAME and atropine sulfate eliminated nearly all of the increases in brachial BFV and vascular conductance during hypothalamic stimulation. From the present results, we conclude that stimulation of the hypothalamic defense area is able to induce neurogenic vasodilatation of the cat forelimb vascular bed, which is greatly mediated with a nitric oxide mechanism. The contribution of nitric oxide to neurogenic vasodilatation seems to be greater in the forelimbs than hindlimbs.