Vagal nerve stimulation increases right ventricular contraction and relaxation and heart rate.
OBJECTIVE
To determine the effects of vasoactive intestinal peptide, released from the right and left vagal nerves, on ventricular contraction, relaxation, and heart rate.


METHODS
The muscarinic and beta-adrenergic receptors were blocked with atropine and propranolol, and afterload was controlled in 48 anesthetized, open-chest mongrel dogs. Experiments were performed in the absence (Series 1, 10 dogs) and in the presence (Series 2, 22 dogs) of a controlled heart rate and prior to and after the administration of a sensitive and selective vasoactive intestinal peptide antagonist (Series 3, 16 dogs).


RESULTS
Right ventricular contraction (+dp/dtmax), relaxation (-dp/dtmin) and heart rate increased significantly during 20 Hz vagal nerve stimulation for 5 min. Vagal nerve stimulation in Series 1 increased right ventricular +dp/dtmax by 28% from a control value of 480 +/- 11 (P < 0.001) and right ventricular -dp/dtmin by 23% from a control value of 341 +/- 11 (P < 0.002). Left ventricular +dp/dtmax and -dp/dtmin increased slightly but not significantly. Vagal nerve stimulation also increased the heart rate by 29% from a control value of 149 +/- 2 (P < 0.001). During controlled heart rate in Series 2, vagal nerve stimulation at 20 Hz consistently increased right ventricular +dp/dtmax and -dp/dtmin comparable to Series 1 experiments but did not increase left ventricular +dp/dtmax or -dp/dtmin. Injection of the vasoactive intestinal peptide antagonist [4Cl-DPhe6, Leu17]VIP into the right coronary artery of 16 dogs in Series 3 did not affect right ventricular +dp/dtmax, -dp/dtmin, or heart rate. However, this antagonist substantially decreased the vagal-induced increases in right ventricular +dp/dtmax, -dp/dtmin, and heart rate by 85, 63, and 71% (P < 0.005), respectively.


CONCLUSIONS
The present experiments suggest that vagal nerve stimulation releases vasoactive intestinal peptide (VIP) or a "VIP-like substance' that significantly increases right ventricular contraction, relaxation, and heart rate.
Henning
R J
RJ
University of South Florida College of Medicine, Division of Cardiology, Tampa, FL, USA.
Feliciano
L
L
Coers
C M
CM
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006727:Hormone Antagonists / Q000494:pharmacology*; D018727:Muscarinic Antagonists / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D018005:Receptors, Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors; D014630:Vagus Nerve / Q000502:physiology*; D014660:Vasoactive Intestinal Peptide / Q000031:analogs & derivatives* / Q000494:pharmacology; D016278:Ventricular Function, Right / Q000502:physiology*
D000319:Adrenergic beta-Antagonists; D006727:Hormone Antagonists; D018727:Muscarinic Antagonists; D018005:Receptors, Vasoactive Intestinal Peptide; C048507:vasoactive intestinal peptide, 4-chloro-Phe(6)-Leu(17)-; D014660:Vasoactive Intestinal Peptide; D001285:Atropine; D011433:Propranolol