Effects of acetylcholine on the heart

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Abstract
In anesthetized open-chest dogs, left ventricular output, coronary sinus outflow, arterial blood pressure, myocardial contractile force, and heart rate were measured. Drugs were injected into the total coronary artery inflow. With acetylcholine chloride, the threshold dose for coronary vasodilating effect (CVD) was 0.01-0.1 [mu]g; for negative inotropic effect it was 10 times the CVD threshold dose; and for negative chronotropic effect, 100 times the CVD threshold dose. After neostigmine, the dose of acetylcholine which caused the negative inotropic and chronotropic effects was reduced to or towards the initial CVD threshold dose. Hence, the initial wide range of threshold doses appeared to be largely explained by differences in cholin-esterase activity near receptor sites. Atropine sulfate, 0.1-0.2 mg, had selective blocking actions on the 3 effects of acetylcholine, varying in extent and duration; larger doses, 1 mg, blocked all 3 effects. Following atropine and neostigmine, 20-300 [mu]g acetylcholine produced a positive inotropic effect which could be blocked by pro-nethalol, dichloroisoproterenol, and tetraethylammonium chloride. The positive inotropic effect appeared to be mediated by a cholinergic mechanism in the release of norepinephrine from sympathetic nerve endings in the heart.

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