The present experiments suggest that VNS releases VIP which directly dilates coronary arteries and significantly increases coronary artery blood flow.

Summary: Acute myocardial ischemia, which results from a significant imbalance between myocardial oxygen demands and myocardial oxygen supply, occurs in as many as six million persons with atherosclerotic coronary artery disease in the United States. Accordingly, a clear understanding of the physiologic and pathophysiologic factors that influence coronary artery blood flow is important to the clinician and provides the basis for the judicious use of medications for the treatment of patients with atherosclerotic coronary artery disease. This review discusses the endothelial, metablic, myogenic, and neurohumoral mechanisms of coronary blood flow regulation and the interaction of the different mechanisms in the regulation of coronary blood flow. The importance of nitric oxide in coronary blood flow regulation is emphasized. We also discuss the common clinical problems of hyperlipidemia and coronary atherosclerosis, coronary artery spasm, and systemic arterial hypertension that result in coronary artery endothelial dysfunction, the impaired production and increased inactivation of nitric oxide, and impairment in coronary blood flow regulation. This information is important to clinicians because more than forty million people in the United States have atherosclerotic or hypertensive heart disease and therefore are at risk for significant myocardial complications due to impairment of coronary blood flow regulation.

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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.

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