Tadayoshi Takeuchi*, Masahiro Sumiyoshi, Munenori Kitayama, Nobue Hirayama, Akikazu Fujita and Fumiaki Hata
Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, Osaka Prefecture University, Sakai 599-8531, Japan
*Corresponding author. FAX: +81-72-254-9480, E-mail: email@example.com
Abstract: The origin of Ca2+ necessary for carbachol (CCh)-induced contraction of longitudinal muscle of the proximal colon of rats was studied. CCh induced contraction of the muscle consisting of two phases, phasic and tonic phases, with a concomitant biphasic increase in [Ca2+]i. After removal of Ca2+ from the bathing solution of the colonic segments, CCh-induced contraction was rapidly inhibited; there was almost complete inhibition 1 min after the removal. Nicardipine, a blocker of voltage-dependent calcium channel, also significantly inhibited CCh-induced contraction. On the other hand, treatment of the colonic segments with thapsigargin, an inhibitor of sarcoplasmic reticulum (SR) Ca2+-ATPase, did not significantly affect the contraction except causing a slight decrease in the rate of contraction. These results suggest that Ca2+ entering through voltage-dependent calcium channels, but not released from SR, is essential for CCh-induced contraction of longitudinal muscle of the proximal colon of rats. This strict dependency of the CCh-induced contraction on extracellular Ca2+ was discussed in relation to the results obtained in the fundus of rats.
Keywords: Rat proximal colon, Origin of calcium, Voltage-dependent calcium channel, Sarcoplasmic reticulum
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