Abstract
In summary, the present study is further evidence for an interaction of angiotensin with adrenergic neurons in the myocardium. Concentrations of the peptides which do not display inotropic activity in point-stimulated atria result in marked facilitation of the release of neurotransmitter and DβH from adrenergic neurons in field-stimulated atrial preparations. The neuronal receptor for angiotensin is relatively resistant to blockade with an angiotensin antagonist, saralasin.
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