Abstract
SummaryThe accelerator response to sympathetic nerve stimulation in perfused rabbit hearts was significantly greater during than before angiotensin infusions. A similar effect of angiotensin at other adrenergic neuroeffector sites has been reported previously, and mechanisms of action that have been suggested for this influence include sensitization of the receptor site to the action of norepinephrine, prevention of the re-uptake or facilitated release of norepinephrine. Evidence is presented in the experiments reported here that at cardiac neuroeffector sites angiotensin does not sensitize the receptor sites nor prevent the uptake of norepinephrine, since the accelerator responses to norepinephrine were similar before and during angiotensin infusions. It appears most likely, therefore, that the mechanism by which angiotensin causes an increased accelerator response to sympathetic nerve stimulation in these preparations is to potentiate the release of norepinephrine from the active adrenergic nerve endings.
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