Particulate guanylyl cyclase and cholinergic control of cardiac excitability is site specific.

We read with interest the recent study by Imai et al. [7] citability is controversial. Han et al. [3] first proposed that who provide evidence that muscarinic inhibition of prestimulation of muscarinic receptors in sinoatrial node cells stimulated L-type calcium current (I ) may involve an increases nitric oxide (NO) production via endothelial NO CaL increase in cGMP levels via particulate guanylyl cyclase. synthase (eNOS). Stimulation of soluble guanylyl cyclase This mechanism is apparent when cAMP has been raised was essential for cholinergic inhibition of L-type calcium by inhibition of phosphodiesterase. The role of the cGMP current (I ) following adrenergic pre-stimulation, alCaL pathway in the cholinergic modulation of cardiac exthough others fail to confirm this result (e.g. Refs. [2,8,9]).