A role of nitric oxide in vasomotor control of cerebral parenchymal arterioles in rats

Abstract

The present study was undertaken to determine the role of nitric oxide (NO) in the regulation of vasomotor tone in rat cerebral parenchymal arterioles under physiological and pathological conditions. Cerebral arterioles, about 60 μm in diameter, were isolated from rats and cannulated with glass pipettes. Changes in the arteriolar diameter secondary to extraluminal application of drugs were monitored continuously through a videodimension analysis system. The arterioles were dilated by l-arginine (12.2 ± 2.2% at 10 −3 M) and were constricted by N G-monomethyl- l-arginine ( l-NMMA) (13.8 ± 1.5% at 10 −4 M) in a dose-dependent manner. Pretreatment with superoxide dismutase (600 U) increased sensitivity to l-arginine. These results suggest that NO plays an important role in regulation of basal vasomotor tone of cerebral parenchymal arterioles under physiological conditions. Next, NO-modification of vasomotor responses to an endogenous vasoactive substance, arginine vasopressin (AVP) was studied in cerebral parenchymal arterioles. Increasing concentrations of AVP produced biphasic responses of vasodilation (10 −11 M) and vasoconstriction (10 −10 − 10 −8 M). Inhibition of NO by pretreatment with l-NMMA (10 −4 M) or oxyhemoglobin (10 −5 M) abolished the vasodilation and enhanced the vasoconstriction by AVP. Therefore, under pathological conditions in which NO function was suppressed, such endogenous substances may produce contraction in parenchymal arterioles instead of dilation with aggravation of cerebral ischemia.