Effects of adrenoceptor stimulating and blocking agents on carotid body chemosensory inhibition

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Abstract
The effects of .alpha.- and .beta.-adrenoceptor agonists and antagonists on chemosensory discharges originating from carotid bodies in situ were studied in anesthetized cats. Noradrenaline (norepinephrine, NA) injections commonly resulted in increased frequency of carotid nerve chemosensory discharge, an effect ascribed to reduced blood flow through the glomus, and reduced or eliminated by .alpha.-adrenergic block. NA injections occasionally produced an initial reduction of chemosensory discharge frequency, which was less intense and of shorter duration than that caused by dopamine. This effect of NA is not mediated by .alpha.-adrenoceptors, since it is not blocked by dibenamine, but probably by low affinity for dopamine receptors. Dopamine and apomorphine-elicited chemosensory inhibition were not affected by low doses of phenoxybenzamine, which blocked NA-evoked hypertensive reactions. Higher doses of phenoxybenzamine and dibenamine produced a displacement to the right of dose-response curves for dopamine- and apormorphine-elicited chemosensory inhibition. This interference by .alpha.-adrenergic blockers was attributed to the resultant hypotension, since it was reversed on restoration of blood pressure. Isoprenaline, a .beta.-adrenergic agonist, did not induce chemosensory inhibition, while .beta.-adrenergic blockers (propranolol and dichloroisoproterenol) did not modify dopamine- and apomorphine-elicited chemosensory inhibition. Further support for the hypothesis that chemosensory inhibition could be mediated by specific dopamine receptors, distinct from .alpha.- and .beta.-adrenoceptors was provided.