A. NAJAFI-FARASHAH A. ENDOGENOUS RELEASE OF OPIATES BY REPETITIVE ELECTRICAL FIELD STIMULATION IN THE GUINEA-PIG AND RAT ILEAL LONGITUDINAL MUSCLE. Med J Islam Repub Iran 1990; 4 (1) :53-59
URL:
http://mjiri.iums.ac.ir/article-1-1571-en.html
From the Department of Physiology, Medical School, Yazd University of Medical Sciences, Yazd, Islamic Republic of Iran.
Abstract: (4199 Views)
The effect of repetitive electrical field stimulation and the response of
the guinea-pig and rat ileal longitudinal muscle to single pulse stimulations
was examined. Single pulse field stimulation produced twitch contraction
which was inhibited by repetitive field stimulation (10 Hz, 40V, 0.5 msec for 5
m). This inhibition was largely, though never completely, reversed by
naloxone. Contractions due to exogenous acetylcholine and histamine were
also inhibited after repetitive field stimulation. The inhibition of acetylcholine
response was party reversed by naloxone whereas that of histamine was
not. Contractions due to single pulse field stimulation or to either acetylcholine
or histamine were inhibited by prior exposure to high concentrations of
acetylcholine as a substitute for high frequency stimulation. The inhibitory
responses were resistant to naloxone. The inhibitory responses to acetylcholine
and histamine after exposure to the lowest concentration of acetylcholine
was seen in preparations treated with tetrodotoxin or hemicholinium.
The inhibition of the histamine response by acetylcholine pretreatment was
prevented by mepyramine. Response to histamine, but not those to single
pulse field stimulation or acetylcholine, were inhibited by prior exposure to
histamine. It is concluded that repetitive field stimulation possibly initiates
two distinct inhibitory processes. One involves the release of endogenous
opiates and is probably mediated by inhibition of acetylcholine release. The
second type of inhibition is not mediated by endogenous opiates and can be
explained by post-junctional desensitization. The non-specific desensitization
to histamine is probably a consequence of histamine release from mast
cells by acetylcholine.