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AJP - Heart and Circulatory Physiology, Vol 255, Issue 1 207-H212, Copyright © 1988 by American Physiological Society
ARTICLES |
K. Komori, R. R. Lorenz and P. M. Vanhoutte
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905.
The effects of nitric oxide and acetylcholine (ACh) were investigated on the electrical and mechanical properties of vascular smooth muscle cells of the canine mesenteric artery. Isolated tissues with or without the endothelium were contracted with prostaglandin F2 alpha. Nitric oxide caused comparable concentration-dependent relaxations in rings with and without endothelium. ACh induced concentration-dependent relaxations only in arteries with endothelium. The relaxations to both nitric oxide and ACh were inhibited by methylene blue or oxyhemoglobin. Either in the presence or absence of prostaglandin F2 alpha, ACh caused transient hyperpolarization of the cell membrane of the vascular smooth muscle. The ACh-induced transient hyperpolarization was not observed after mechanical removal of the endothelial cells or after treatment with atropine. Nitric oxide (less than or equal to 8 X 10(-6) M) did not alter membrane potential, in either the presence or absence of the endothelium. The excitatory junction potentials generated by perivascular nerve stimulation were inhibited by ACh but not by nitric oxide. These results suggest that in the canine mesenteric artery 1) the endothelium-derived hyperpolarizing factor generated by ACh is not nitric oxide; 2) nitric oxide relaxes vascular smooth muscle by a direct effect; and 3) nitric oxide does not modify adrenergic neurotransmission.
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