Electrical responses of gastric smooth muscles in streptozotocin
-induced diabetic rats.
Xue, Lin, and Hikaru Suzuki.
Department of Physiology, Nagoya City University Medical School,
Mizuho-ku, Nagoya 467, Japan.
APStracts 3:0147G, 1996.
Electrical responses of gastric smooth muscles produced by transmural
nerve stimulation, acetylcholine, norepinephrine or K-free solution
were investigated in streptozotocin-induced diabetic rats, using
intracellular microelectrode techniques. In muscles from diabetic
rats, 1) the resting membrane potential remained unchanged, 2) slow
waves either disappeared or were markedly reduced in amplitude, 3)
the excitatory junction potential was absent, and in most cases only
an inhibitory junction potential of reduced amplitude was elicited,
4) the amplitude of the hyperpolarization generated after superfusion
with K-free solution was reduced, 5) the sensitivity of the
acetylcholine-induced membrane depolarization was increased, and 6)
the norepinephrine-induced hyperpolarization was reduced, due to
functional loss of both alpha- and beta-adrenoceptors. Thus, diabetes
mellitus caused functional impairment of neuromuscular transmission,
reduced maximum activity of the electrogenic pump, increased the
sensitivity of muscarinic receptors, reduced the sensitivity of
adrenoceptors and reduced the myogenic activity in gastric smooth
muscles. These alterations of the properties of smooth muscle may be
involved in the diabetes-induced gastroparesis.
Received 16 October 1995; accepted in final form 18 July 1996.
APS Manuscript Number G449-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996