Modulation of the release of [3H]norepinephrine from the base and body of the rat urinary bladder by endogenous adrenergic and cholinergic mechanisms

GT Somogyi and WC de Groat

Department of Pharmacology, University of Pittsburgh, Pennsylvania.

Modulation of [3H]NE release was studied in rat urinary bladder strips prelabeled with [3H]NE. [3H]NE uptake occurred in strips from the bladder base and body, but was very prominent in the base where the noradrenergic innervation is most dense. Electrical field stimulation markedly increased [3H]NE outflow from the superfused tissue. The quantity of [3H]NE release was approximately equal during three consecutive periods of stimulation. Activation of presynaptic muscarinic receptors by 1.0 microM oxotremorine reduced [3H]NE release to 46% of the control. Atropine (1 microM) blocked the effect of oxotremorine and increased the release to 147% of predrug control levels. Activation of presynaptic alpha-2 adrenoceptors by 1 microM clonidine reduced [3H]NE release to 55% of control. Yohimbine blocked the action of clonidine and increased the release to 148% of control. The release of [3H]NE from the bladder base and body was increased by both 1 microM atropine (to 167% and 174% of control, respectively) and 1 microM yohimbine (to 286% and 425% of control, respectively). Atropine and yohimbine administered in combination had similar facilitatory effects as when administered alone. We conclude that the release of [3H]NE from adrenergic nerve endings in electrically stimulated bladder strips is modulated via endogenous transmitters acting on both muscarinic and alpha-2 adrenergic presynaptic receptors and that the latter provide the most prominent control.

Volume 255, Issue 1, pp. 204-210, 10/01/1990
Copyright © 1990 by American Society for Pharmacology and Experimental Therapeutics