AJP - Regulatory, Integrative and Comparative Physiology, Vol 255, Issue 6 888-R893, Copyright © 1988 by American Physiological Society
Regulation of [3H]GABA release from strips of guinea pig urinary bladder
J. Shirakawa, K. Taniyama, S. Iwai and C. Tanaka
Department of Anesthesiology, Kobe University, School of Medicine, Japan.
The presence of receptors that regulate the release of gamma-aminobutyric
acid (GABA) was studied in strips of the guinea pig urinary bladder. GABA
(10(-8)-10(-5) M) and muscimol (10(-8)-10(-5) M), but not baclofen (10(-5)
M), reduced the Ca2+-dependent, tetrodotoxin-resistant release of [3H]GABA
evoked by high K+ from the urinary bladder strips preloaded with [3H]GABA.
The inhibitory effect of muscimol was antagonized by bicuculline and
potentiated by diazepam, clonazepam, and pentobarbital sodium. The
potentiating effect of clonazepam was antagonized by Ro 15-1788.
Acetylcholine (ACh) inhibited the high K+-evoked release of [3H]GABA. The
inhibitory effect of ACh was antagonized by atropine sulfate and
pirenzepine but not by hexamethonium. Norepinephrine (NE) inhibited the
evoked release of [3H]GABA. The inhibitory effect of NE was mimicked by
clonidine, but not by phenylephrine, and was antagonized by yohimbine but
not by prazosin. These results provide evidence that the release of GABA
from strips of guinea pig urinary bladder is regulated via the
bicuculline-sensitive GABAA receptor, M1-muscarinic, and alpha 2-adrenergic
receptors.
