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Am J Physiol Regul Integr Comp Physiol 262: R400-R406, 1992;
0363-6119/92 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 262, Issue 3 400-R406, Copyright © 1992 by American Physiological Society

ARTICLES

Adrenergic presynaptic antagonists and their mechanism of action in smooth muscle

S. Kalsner
Department of Physiology, City University of New York Medical School, City College of New York, New York 10031.

The effects of veratridine and of yohimbine on the efflux of norepinephrine from guinea pig ureters was examined to gain insight into presynaptic receptor function. Ureter segments were stimulated at 1 and 2 Hz with 100 pulses in the absence and presence of yohimbine, veratridine, or the combination. Veratridine (4.5 or 6 x 10(-7) M) increased transmitter release. The enhancements of release by the adrenergic antagonist yohimbine and by veratridine were not additive, suggesting a common site of action. The lack of additivity was not linked to a ceiling effect since tetraethylammonium, which increases release by block of potassium channels, had an additive effect with veratridine. Protection experiments, done with veratridine as the protecting agent against phenoxybenzamine blockade, supported the interpretation that adrenergic antagonists and veratridine act at a common locus to enhance transmitter efflux. Although veratridine enhanced transmitter efflux like yohimbine, it only slightly reduced the inhibitory capacity of norepinephrine, confirming the likelihood of discrete sites of agonist and antagonist action. Veratridine and alpha-receptor antagonists might combine presynaptically with sites on the sodium channels of sympathetic nerve terminals to alter channel gating, namely the shifting of sodium channel activation to more negative potentials, and in this way increase the liberation of norepinephrine.


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