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We tested the hypothesis that strain is the primary mechanical signal in the mechanosensitive modulation of intracellular Ca 2+ concentration ([Ca 2+ ] i ) in airway smooth muscle. We found that [Ca 2+ ] i  was significantly correlated with muscle length during isotonic shortening against 20% isometric force (F iso ). When the isotonic load was changed to 50% F iso , data points from the 20 and 50% F iso  experiments overlapped in the length-[Ca 2+ ] i  relationship. Similarly, data points from the 80% F iso  experiments clustered near those from the 50% F iso  experiments. Therefore, despite 2.5- and 4-fold differences in external load, [Ca 2+ ] i did not deviate much from the length-[Ca 2+ ] i relation that fitted the 20% F iso  data. Maximal inhibition of sarcoplasmic reticular (SR) Ca 2+  uptake by 10 μM cyclopiazonic acid (CPA) did not significantly change [Ca 2+ ] 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 ( L  o ) to 0.5 L  o . These results are consistent with the hypothesis and suggest that SR Ca 2+  uptake is not the underlying mechanism.

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

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