Effects of adrenoceptor stimulating and blocking agents on carotid body chemosensory inhibition.
1. The effects of alpha- and beta-adrenoceptor agonists and antagonists on chemosensory discharges originating from carotid bodies in situ were studied in anaesthetized cats.2. Noradrenaline (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.3. NA injections occasionally produced an initial reduction of chemosensory discharge frequency, which was however 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.4. Dopamine and apomorphine-elicited chemosensory inhibition were not affected by low doses of phenoxybenzamine, which blocked NA-evoked hypertensive reactions.5. Higher doses of phenoxybenzamine and dibenamine produced a displacement to the right of dose-response curves for dopamine- and apormorphine-elicited chemosensory inhibition. However, this interference by alpha-adrenergic blockers was attributed to the resultant hypotension, since it was reversed upon restoration of blood pressure.6. Isoprenaline, a beta-adrenergic agonist, did not induce chemosensory inhibition, whilst beta-adrenergic blockers (propranolol and dichloroisoproterenol) did not modify dopamine- and apomorphine-elicited chemosensory inhibition.7. These results provide further support for the hypothesis that chemosensory inhibition could be mediated by specific dopamine receptors, distinct from alpha- and beta-adrenoceptors.
Effects of adrenoceptor stimulating and blocking agents on carotid body chemosensory inhibition. 1. The effects of alpha- and beta-adrenoceptor agonists and antagonists on chemosensory discharges originating from carotid bodies in situ were studied in anaesthetized cats.2. Noradrenaline (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.3. NA injections occasionally produced an initial reduction of chemosensory discharge frequency, which was however 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.4. Dopamine and apomorphine-elicited chemosensory inhibition were not affected by low doses of phenoxybenzamine, which blocked NA-evoked hypertensive reactions.5. Higher doses of phenoxybenzamine and dibenamine produced a displacement to the right of dose-response curves for dopamine- and apormorphine-elicited chemosensory inhibition. However, this interference by alpha-adrenergic blockers was attributed to the resultant hypotension, since it was reversed upon restoration of blood pressure.6. Isoprenaline, a beta-adrenergic agonist, did not induce chemosensory inhibition, whilst beta-adrenergic blockers (propranolol and dichloroisoproterenol) did not modify dopamine- and apomorphine-elicited chemosensory inhibition.7. These results provide further support for the hypothesis that chemosensory inhibition could be mediated by specific dopamine receptors, distinct from alpha- and beta-adrenoceptors.