Vasoactive intestinal polypeptide facilitates atrioventricular nodal conduction and shortens atrial and ventricular refractory periods in conscious and anesthetized dogs.

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Abstract
Our study was designed to determine the cardiac electrophysiological influence of vasoactive intestinal polypeptide (VIP) in conscious dogs. Dogs (n = 8) were chronically instrumented with arterial and venous catheters, cervical vagal cooling coils, and right atrial and right ventricular bipolar epicardial pacing and recording electrodes. After autonomic blockade (10 mg/kg i.v. hexamethonium, 0.11 mg/kg i.v. atropine, and vagal cold blockade), VIP (50 and 100 pmol/kg/min i.v.) or isoproterenol (ISO) (250 and 500 pmol/kg/min i.v.) increased heart rate (maximum increases: VIP, 81.1 .+-. 4.2 beats/min; ISO, 61.3 .+-. 8.5 beats/min), decreased the atrial-ventricular interval (during constant atrial pacing) (VIP, -41.9 .+-. 6.3 msec; ISO,-34.6 .+-. 7.4 msec), shortened the atrial effective refractory period (VIP, -24.4 .+-. 2.1 msec; ISO,-30.6 .+-. 4.4 msec) and ventricular effective refractory period (VIP, -4.2 .+-. 0.7 msec; ISO, -10.0 .+-. 2.4 msec), and decreased mean arterial pressure (VIP, -51.9 .+-. 4.0 mm Hg; ISO, -26.1 .+-. 2.4 mm Hg). .beta.-Adrenergic blockade with propranolol (1 mg/kg i.v.) eliminated the positive chronotropic and atrioventricular nodal dromotropic responses to bolus doses of ISO (30, 100, 300, and 1,000 pmol/kg i.v.) but did not affect the responses to VIP (10, 30, 100, and 300 pmol/kg i.v.). Comparable blood pressure decreases produced by sodium nitroprusside caused only minimal changes in heart rate, atrial-ventricular conduction times, and atrial and ventricular refractory periods. In three additional anesthetized dogs, after vagotomy and .beta.-adrenergic blockade (1 mg/kg i.v. propranolol), VIP (100 pmol/kg/min i.v.) shortened the atrial-His interval but did not alter intra-atrial, intraventricular, or His-Purkinje conduction. Our findings combined with the demonstration by other of VIP-immunoreactive nerves innervating canine sinus nodal cells, atrioventricular nodal cells, and atrial and ventricular myocardial cells suggest that endogenous VIP may directly alter the electrical properties of the heart.