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The role of sarcoplasmic reticulum and sarcoplasmic reticulum Ca-2+-ATPase in the smooth muscle tone of the cat gastric fundus



The role of sarcoplasmic reticulum and sarcoplasmic reticulum Ca-2+-ATPase in the smooth muscle tone of the cat gastric fundus



Pfluegers Archiv European Journal of Physiology 431(6): 928-935



Circular smooth muscle strips isolated from cat gastric fundus were studied in order to understand whether the sarcoplasmic reticulum (SR) and SR Ca-2+-ATPase could play a role in the regulation of the muscle tone. Cyclopiazonic acid (CPA), a specific inhibitor of SR Ca-2+-ATPase, caused a significant and sustained increase in muscle tone, depending on the presence of extracellular Ca-2+. Nifedipine and cinnarizin only partially suppressed the CPA-induced tonic contraction. Bay K 8644 antagonized the relaxant effect of nifedipine in CPA-contracted fundus. Nitric-oxide-releasing agents sodium nitroprusside and 3-morpholino-sydnonimine completely suppressed the CPA-induced tonic contraction. The blockers of Ca-2+-activated K+ channels, tetraethylammonium, charybdotoxin and/or apamin, decreased the contractile effect of CPA. Vanadate increased the tone but did not change significantly the effect of CPA. CPA exerted its contractile effect even when Ca-2+ influx was triggered through the Na+/Ca-2+ exchanger and the other Ca-2+ entry pathways were blocked. Thapsigargin, another specific SR Ca-2+-ATPase inhibitor, also increased the muscle tone. The effect of thapsigargin was completely suppressed by sodium nitroprusside and 3-morpholino-sydnonimine and partially by nifedipine. In conclusion, under conditions when the SR Ca-2+-ATPase is inhibited, the tissue develops a strong tonic contraction and a large part of this is mediated by Ca-2+ influx presumably via nifedipine-sensitive Ca-2+ channels. This study suggests the important role of SR Ca-2+-ATPase in the modulation of the muscle tone and the function of SR as a "buffer barrier" to Ca-2+ entry in the cat gastric fundus smooth muscle.

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Accession: 009622222

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PMID: 8927511

DOI: 10.1007/bf02332179


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