Abstract

In spite of the relatively large amount of in vitro and in vivo data indicating that, in a number of ways, cerebral arteries are pharmacologically different from peripheral arteries, the mechanisms responsible for these differences are far from clear. An understanding of these mechanisms is particularly important for a rational approach to the treatment of disorders of the cerebral circulation including migraine, hypertension and the responses of cerebral vessels to subarachnoid haemorrhage. This review outlines electrophysiological data which are available from cerebrovascular smooth muscle cells, including the possibility that inwardly-rectifying potassium channels, active a potentials close to the resting membrane potential, are intimately involved in the changes in smooth muscle tone which couple blood flow to regional changes in nerve cell activity. The membrane potential changes in response to perivascular nerve stimulation, noradrenaline, 5-hydroxytryptamine and endothelium-derived hyperpolarizing factor are also described, together with the underlying membrane mechanisms and their relationship to smooth muscle contraction and relaxation.

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