Angiotensin II on the release of DbetaH and atrial cyclic AMP concentrations

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Abstract
The cardiac effects of angiotensin mediated by myocardial sympathetic neurons were studied in isolated rabbit left atria by comparing the effect of the peptide on field-(nerve and muscle)-stimulated and point-(muscle)-stimulated atria paced at 96 beats/min in modified oxygenated Krebs buffer at 30.degree. C. Using the indirectly acting sympathomimetic agent, tyramine, and the .beta.-adrenergic blocking agent, propranolol, evidence was obtained that angiotensin potentiated the responses to sympathetic nerve stimulation. At a concentration that maximally facilitated inotropic responses of field-stimulated atria to tyramine, angiotensin (1 .times. 10-10 M) increased atrial cyclic[c]AMP levels only during sympathetic nerve stimulation. This cAMP response was attenuated by propranolol. In concentrations greater than 3 .times. 10-11 M, angiotensin II caused a dose-dependent increase in dopamine .beta.-hydroxylase activity only in the baths of field-stimulated atria. This effect of angiotensin on atrial sympathetic neurons was antagonized competitively by saralasin (3 .times. 10-8 M). The concomitant administration of angiotensin and tyramine during field stimulation produced a greater rise in cAMP levels than was obtained with either compound alone. In concentrations which do not produce a direct inotropic response of the isolated rabbit atrium, angiotensin enhances the effects of sympathetic nerve stimulation.