Histamine potentiation of nerve- and drug-induced responses of a rabbit cerebral artery.

Abstract

Rabbit basilar artery rings are normally relatively unresponsive to transmural stimulation of their sympathetic nerve supply. However, in the presence of histamine (0.55 /i M )> contractile responses to nerve stimulation were markedly increased. Norepinephrine and serotonin concentrations that produce 50% of a maximum contractile response (ED 50 ) were considerably decreased in the presence of histamine; maximum responses to both norepinephrine and serotonin were increased. Although a prejunctional effect of histamine has not been eliminated, potentiation of responses to transmural nerve stimulation is probably due to an increase in smooth muscle responsiveness to norepinephrine. In rabbit saphenous artery rings, histamine produced a qualitatively similar potentiation of responses to nerve stimulation, norepinephrine, and serotonin except that maximum responses were not increased. Serotonin (0.084 JJM) did not potentiate contractile responses of the basilar artery to transmural nerve stimulation or norepinephrine. Since histamine and serotonin are released from rabbit platelets in response to tissue injury, the synergistic effect of these agents on vascular smooth muscle contraction might be advantageous in minimizing hemorrhage. But such a response could also be deleterious if the effects of these vasoconstrictors were prolonged. KEY WORDSnorepinephrine serotonin cerebral vasospasm hemorrhage nervous control of cerebral circulation saphenous artery basilar artery• Numerous studies of the physiology and pharmacology of the cerebral vasculature have been reported, yet controversy over the control of brain blood flow continues (1). This is especially true of nervous control of the cerebral circulation. Although an adequate sympathetic nerve supply to the larger cerebral arteries has been demonstrated by morphological techniques (2-4), its functional significance is still in doubt. Carefully designed studies in dogs have shown a decrease in cerebral blood flow with adrenergic nerve stimulation, although the high rates of stimulation which are necessary to elicit measurable changes cast some doubt on the relevance of this finding (5). Cerebral arteries have a low sensitivity to lnorepinephrine in comparison with that of other vessels (6, 7). Although cerebral arteries contract in vitro when their intramural nerves are stimulated electrically, this response is small in comparison This investigation was supported by U. S. Public Health Service Grant HL15805 from the National Heart and Lung Institute and by Grant 408 IG from the Los Angeles County Heart Association. Dr. Duckies is a Los Angeles County Heart Association postdoctoral fellow, and Dr. Lee is a U. S. Public Health Service postdoctoral fellow supported by Grant NS 2040. Received October, 15, 1974. Accepted for publication February 27, 1975. with that of other vessels (8); moreover, some workers have been unable to demonstrate a response in some species (7).Because of the uncertainty about nervous control of the cerebral circulation, we were inter...

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