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

Steven S. An, Chi Ming Hai

Research output: Contribution to journalArticlepeer-review

Abstract

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 (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-[Ca2+](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, [Ca2+](i) did not deviate much from the length-[Ca2+](i) relation that fitted the 20% F(iso) 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.

Original languageEnglish (US)
Pages (from-to)C1375-C1384
JournalAmerican Journal of Physiology - Cell Physiology
Volume279
Issue number5 48-5
DOIs
StatePublished - 2000
Externally publishedYes

Keywords

  • Acetylcholine
  • Calcium
  • Intracellular calcium concentration
  • Mechanotransduction
  • Muscle length

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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