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Rigel DF, Lathrop DA. Vasoactive intestinal polypeptide facilitates atrioventricular nodal conduction and shortens atrial and ventricular refractory periods in conscious and anesthetized dogs. Circ Res. 1990;67(6):1323-33doi: 10.1161/01.res.67.6.1323.
Rigel, D. F., & Lathrop, D. A. (1990). Vasoactive intestinal polypeptide facilitates atrioventricular nodal conduction and shortens atrial and ventricular refractory periods in conscious and anesthetized dogs. Circulation research, 67(6), 1323-33. https://doi.org/10.1161/01.res.67.6.1323
Rigel, D F, and Lathrop, D A. "Vasoactive intestinal polypeptide facilitates atrioventricular nodal conduction and shortens atrial and ventricular refractory periods in conscious and anesthetized dogs." Circulation research vol. 67,6 (1990): 1323-33. doi: https://doi.org/10.1161/01.res.67.6.1323
Rigel DF, Lathrop DA. Vasoactive intestinal polypeptide facilitates atrioventricular nodal conduction and shortens atrial and ventricular refractory periods in conscious and anesthetized dogs. Circ Res. 1990 Dec;67(6):1323-33. doi: 10.1161/01.res.67.6.1323. PMID: 2245498.
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Circ Res. 1990 Dec;67(6):1323-33. doi: 10.1161/01.res.67.6.1323.

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

Circulation research

D F Rigel, D A Lathrop

Affiliations

  1. Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Ohio.

PMID: 2245498 DOI: 10.1161/01.res.67.6.1323

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 others 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.

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