Effects of pituitary adenylate cyclase-activating polypeptide on canine atrial electrophysiology

We hypothesized that pituitary adenylate cyclase-activating polypeptide (PA CAP) activates intracardiac postganglionic parasympathetic nerves and has a different effect than cervical vagal stimulation. We measured effective re fractory period (ERP) and conduction velocity at four atrial sites [high ri ght atrium (HRA), low right atrium (LRA), high left atrium (HLA), and low l eft atrium (LLA)] and minimum atrial fibrillation (AF) cycle length at 12 a trial sites during cervical vagal stimulation and after PACAP in 26 autonom ically decentralized, open-chest, anesthetized dogs. PACAP shortened ERP to a similar extent at all four sites (HRA, 58 +/- 2.0 ms; LRA, 60 +/- 6.3 ms ; HLA, 68 +/- 11.5 ms; and LLA, 60 +/- 8.3 ms). Low- and high-intensity vag al stimulation shortened ERP at the HRA, but not in the other atrial sites (low-intensity stimulation: HRA, 64 +/- 4.0 ms; LRA, 126 +/- 5.1 ms; HLA, 1 10 +/- 9.5 ms; and LLA, 102 +/- 11.5 ms; high-intensity stimulation: HRA, 5 8 +/- 4.2 ms; and HLA, 101 +/- 4.0 ins). Conduction velocity was not altere d by any intervention. Minimum AF cycle length after PACAP was similar in b oth atria but was shorter in the right atrium than in the left atrium durin g vagal stimulation. After atropine administration, no interventions change d ERP. These results suggest that PACA-P shortens atrial refractoriness uni formly in both atria through activation of intrinsic cardiac nerves, not al l of which are activated by cervical vagal stimulation.