In this study we

Vasoactive intestinal polypeptide, a neurotransmitter peptide detected in animal and human hearts, has been found in nerves of coronary arteries. To determine the amount and distribution of vasoactive intestinal polypeptide in the large coronary vessels and its possible participation in coronary vasoregulation, two groups of animals were studied. In the first group, 11 anesthetized dogs were sacrificed to collect three (1 cm) segments along the circumflex and left anterior descending coronary arteries. These segments represented proximal (I), middle (II) and distal (III) portions of the two arteries. Concentrations (ng/g) of vasoactive intestinal polypeptide-like immunoreactive substance were determined by radioimmunoassay. Vasoactive intestinal polypeptide-like immunoreactivity was present in the left anterior descending (I = 7.28 +/- 1.65, II = 3.74 +/- 0.57, III = 2.29 +/- 0.53) and circumflex (I = 4.16 +/- 1.52, II = 4.58 +/- 1.13, III = 4.00 +/- 0.81) coronary arteries. The difference in vasoactive intestinal polypeptide-like immunoreactivity among epicardial segments of the anterior descending artery was significant, but there was no significant difference among segments of the circumflex coronary artery. In the second group (eight closed chest anesthetized dogs), the effects of vasoactive intestinal polypeptide intracoronary infusion on epicardial coronary constriction were examined at rest and with the artery constricted by serotonin. Left anterior descending (segments I, II and III) artery responses (% area change) to vasoactive intestinal polypeptide and vasoactive intestinal polypeptide plus serotonin were examined using quantitative coronary angiography. Vasoactive intestinal polypeptide infusion resulted in significant vasodilation in all the segments (I, II and III) of the left anterior descending artery.(ABSTRACT TRUNCATED AT 250 WORDS)

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To determine the role of sympathetic innervation on nicotine-induced alterations in peripheral (hindlimb) blood flow in the pentobarbital-anesthetized dog, one hindlimb was acutely denervated and remained attached to the body by only the femoral artery and vein, whereas the contralateral limb remained innervated and intact. Measurements were made of aortic pressure, femoral artery and venous pressures, femoral artery flow, and plasma catecholamine levels during intravenous systemic infusion of nicotine. The response to nicotine (9-36 micrograms.kg-1.min-1) on the denervated side was a transient increase followed by a persistent decrease in flow and increase in vascular resistance. The response in the innervated limb was a large increase in blood flow and decrease in vascular resistance. The vasoconstrictor and vasodilator responses could be abolished by pretreatment with both propranolol and phentolamine. The vasodilator response could not be abolished by cholinergic or histaminergic receptor antagonism. Hexamethonium abolished all systemic and peripheral responses to nicotine. Desipramine selectively abolished the vasodilator response in the innervated hindlimb. The vasodilator and vasoconstrictor responses could be mimicked with systemic or local administration of epinephrine. We conclude that, in the hindlimbs of dogs, nicotine stimulates the release of epinephrine from nerve terminals and/or tissue stores to activate beta 2-adrenoceptors and promote vasodilation in skeletal muscle of innervated preparations.

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