Vagal nerve stimulation increases right ventricular contraction and relaxation and heart rate

Abstract

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

An Investigation into the Presence of a Vagal Tachycardia and the Effect of Vasoactive Intestinal Polypeptide on Rat Heart Rate in vitro

“…The stimulation protocol was repeated at the same frequencies but for a longer duration of 1 min after exposing the atria to atropine (3 mol/l) for 3 min. The reason for the longer electrical stimulation after atropine is that the vagal tachycardia is known to require a longer duration of stimulation [3,7] .…”

“…Nevertheless, the presence of a vagal tachycardia in a species may be a relatively good indicator of the potential physiological contribution of VIP to vagal cardiac function. It is well established that the tachycardia is easily obtainable in the dog [1,3] and it has been shown in the same species that VIP plays a role in the maintenance of normal sinus arrhythmia [4] . However, the exact role of VIP in the vagal regulation of the rat heart has not been established.…”

Vasoactive intestinal peptide has a direct positive inotropic effect on isolated human myocardial trabeculae

“…Cardiac vagal nerve stimulation in dogs during muscarinic and β-adrenergic receptor blockade, caused increased contractile force in the right atrium [4] and the right ventricle [5,6], whereas no significant [5][6][7]. It was also shown that intracoronary infusion of the VIP antagonist [4Cl-D-Phe',Leu"(]VIP could significantly reduce the vagal-induced increases in right atrial\right ventricular contractility, suggesting that VIP was the mediator of this positive inotropic effect in the right atrium and ventricle [4,6,8].…”

An Evaluation of the Efficacy of Vasoactive Intestinal Polypeptide Antagonists in vivo in the Anaesthetized Dog

“…The dose of VIP receptor antagonists used in the present study, 100 Ìg i.c. given to dogs with an average weight of 19.5 kg, was effectively just above 5 mg kg -1 , a concentration which is generally larger than that used by other investigators [10][11][12][15][16][17].…”