期刊
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
卷 280, 期 3, 页码 G439-G448出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.2001.280.3.G439
关键词
pacemaker activity; intestinal motility; cation channel; smooth muscle; interstitial cell of Cajal
Slow waves determine frequency and propagation characteristics of contractions in the small intestine, yet little is known about mechanisms of slow wave regulation. We propose a role for intracellular Ca2+, inositol 1,4,5,-trisphosphate (IP3)-sensitive Ca2+ release, and sarcoplasmic reticulum (SR) Ca2+ content in the regulation of slow wave frequency because 1) 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, a cytosolic Ca2+ chelator, reduced the frequency or abolished the slow waves; 2) thapsigargin and cyclopiazonic acid (CPA), inhibitors of SR Ca2+-ATPase, decreased slow wave frequency; 3) xestospongin C, a reversible, membrane-permeable blocker of IP3-induced Ca2+ release, abolished slow wave activity; 4) caffeine and phospholipase C inhibitors (U-73122, neomycin, and 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate) inhibited slow wave frequency; 5) in the presence of CPA or thapsigargin, stimulation of IP3 synthesis with carbachol, norepinephrine, or phenylephrine acting on alpha (1)-adrenoceptors initially increased slow wave frequency but thereafter increased the rate of frequency decline, 6) thimerosal, a sensitizing agent of IP3 receptors increased slow wave frequency, and 7) ryanodine, a selective modulator of Ca2+ induced Ca2+ release, had no effect on slow wave frequency. In summary, these data are consistent with a role of IP3 sensitive Ca2+ release and the rate of SR Ca2+ refilling in regulation of intestinal slow wave frequency.
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