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We tested the hypothesis that nitric oxide (NO) augments vagal neurotransmission and bradycardia via phosphorylation of presynaptic calcium channels to increase vesicular release of acetylcholine.

The effects of enzyme inhibitors and calcium channel blockers on the actions of the NO donor sodium nitroprusside (SNP) were evaluated in isolated guinea‐pig atrial‐right vagal nerve preparations.

SNP (10 μm) augmented the heart rate response to vagal nerve stimulation but not to the acetylcholine analogue carbamylcholine (100 nm). SNP also increased the release of [³H]acetylcholine in response to field stimulation. No effect of SNP was observed on either the release of [³H] acetylcholine or the HR response to vagal nerve stimulation in the presence of the guanylyl cyclase inhibitor 1H‐(1,2,4)‐oxadiazolo‐(4,3‐a)‐quinoxalin‐1‐one (ODQ, 10 μm).

The phosphodiesterase 3 (PDE 3) inhibitor milrinone (1 …