Key result
Angiotensin facilitates neurotransmitter and DβH release from atrial adrenergic neurons via saralasin-resistant receptors.
Why the study?
Interactions between angiotensin and adrenergic neurons in the myocardium and their effects on neurotransmitter release were not fully understood.
Does angiotensin enhance the release of neurotransmitters from myocardial sympathetic neurons?
Does angiotensin enhance the release of neurotransmitters from myocardial sympathetic neurons?
Angiotensin enhances the release of neurotransmitters from myocardial sympathetic neurons, providing evidence for an interaction between the renin-angiotensin and adrenergic systems in the heart.
Supports angiotensin-adrenergic neuronal interaction in myocardium; extends prior animal evidence but leaves clinical relevance open.
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.
No takes yet. Share an insight, caveat, or question.
Ackerly et al. (1976) studied this question. Angiotensin was evaluated on Release of neurotransmitter and DβH from adrenergic neurons. Angiotensin facilitates the release of neurotransmitter and DβH from adrenergic neurons in atrial preparations, with its neuronal receptor being relatively resistant to saralasin blockade.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: