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Am J Physiol Cell Physiol 279: C1375-C1384, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 5, C1375-C1384, November 2000

Mechanical signals and mechanosensitive modulation of intracellular [Ca2+] in smooth muscle

Steven S. An and Chi-Ming Hai

Department of Molecular Pharmacology, Physiology and Biotechnology, Brown University, Providence, Rhode Island 02912

We tested the hypothesis that strain is the primary mechanical signal in the mechanosensitive modulation of intracellular Ca2+ concentration ([Ca2+]i) in airway smooth muscle. We found that [Ca2+]i was significantly correlated with muscle length during isotonic shortening against 20% isometric force (Fiso). When the isotonic load was changed to 50% Fiso, data points from the 20 and 50% Fiso experiments overlapped in the length-[Ca2+]i relationship. Similarly, data points from the 80% Fiso experiments clustered near those from the 50% Fiso experiments. Therefore, despite 2.5- and 4-fold differences in external load, [Ca2+]i did not deviate much from the length-[Ca2+]i relation that fitted the 20% Fiso data. Maximal inhibition of sarcoplasmic reticular (SR) Ca2+ uptake by 10 µM cyclopiazonic acid (CPA) did not significantly change [Ca2+]i in carbachol-induced isometric contractions and isotonic shortening. CPA also did not significantly change myosin light-chain phosphorylation or force redevelopment when carbachol-activated muscle strips were quickly released from optimal length (Lo) to 0.5 Lo. These results are consistent with the hypothesis and suggest that SR Ca2+ uptake is not the underlying mechanism.

acetylcholine; calcium; intracellular calcium concentration; mechanotransduction; muscle length


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