Neurogenic Dilator and Constrictor Responses of Pial Arteries in Vitro

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Two distinct responses to transmural electrical stimulation of cerebrovascular smooth muscle isolated from dogs and sheep have been identified. Both these responses were blocked with tetrodotoiin and therefore were attributed to stimulation of intramural nerves. A constrictor response to transmural nerve stimulation (TNS) which was blocked with guanethidine was attributed to stimulation of sympathetic nerves. In cerebral arteries of the sheep this constrictor response was blocked by phentolamine, but in dog cerebral vessels it was not. Instead, phentolamine (10′* M) potentiated the response to TNS. Postsynaptic a-adrenergic receptors of dog cerebrovascular smooth muscle may be unusual and hence not susceptible to the action of phentolamine. The increased response to TNS may be due to blockade by phentolamine of presynaptic receptors, causing increased transmitter release. After blockade of the constrictor response to TNS and in the presence of smooth muscle tone, a dilator response, much more prominent in sheep, was unmasked. The dilator response was not blocked by guanethidine, propranolol, or phentolamine, in support of the hypothesis that cerebral vessels are innervated by nonsympathetic nerves. The possibility that these nerves are cholinergic was investigated, but the dilator response was neither blocked by atropine nor potentiated by physostigmine. The nature of the transmitter for this dilator response remains unclear. Some of the marked inconsistencies in studies of neurogenic control of the cerebral circulation may be attributed in part to both qualitative and quantitative differences in neuroeffector mechanisms among species. Circ Reg 44: 482-490, 1979

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