Effects of angiotensin converting enzyme inhibitors and saralasin on noradrenergic and cholinergic transmitter release in guinea pig isolated atria.

The interactions of the converting enzyme inhibitors captopril and enalaprilat and the angiotensin II receptor antagonist saralasin with cardiac autonomic neuroeffector transmission were investigated in guinea pig isolated atria. Noradrenergic transmitter stores were radiolabeled by incubation with [3H]-noradrenaline. In other atria, cholinergic transmitter stores were radiolabeled by incubation with [3H]-choline. Neither captopril nor enalaprilat significantly altered the resting or stimulation-induced (2 Hz, 30 s) efflux of radioactivity in atria that had been incubated with either [3H]-noradrenaline or [3H]-choline. Saralasin also did not significantly alter the resting or stimulation-induced efflux in atria incubated with [3H]-choline. However, in atria incubated with [3H]-noradrenaline, saralasin slightly increased the resting efflux without altering the stimulation-induced efflux. The findings of the present study suggest that neither captopril, enalaprilat, nor saralasin interferes with either noradrenergic or cholinergic transmitter release.