Β3 Adrenoceptor‐induced Cholinergic Inhibition in Human and Rat Urinary Bladders Involves the Exchange Protein Directly Activated by Cyclic AMP 1 Favoring Adenosine Release

The mechanism by which β3 receptor agonists (e.g. mirabegron) control bladder overactivity may involve adenosine release from human and rat detrusor smooth muscle. Retrograde activation of adenosine A1 receptors reduces ACh release from cholinergic bladder nerves. β3‐Adrenoceptors usually couple to adenylyl cyclase. Here we investigated, which of the cAMP targets, protein kinase A or the exchange protein directly activated by cAMP (EPAC) could be involved in this cholinergic inhibition of the bladder.