Mechanical signals and mechanosensitive modulation of intracellular [Ca(2+)] in smooth muscle |
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Authors: | An S S Hai C M |
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Institution: | Department of Molecular Pharmacology, Physiology and Biotechnology, Brown University, Providence, Rhode Island 02912, USA. |
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Abstract: | We testedthe hypothesis that strain is the primary mechanical signal in themechanosensitive modulation of intracellular Ca2+concentration (Ca2+]i) in airway smoothmuscle. We found that Ca2+]i wassignificantly correlated with muscle length during isotonic shorteningagainst 20% isometric force (Fiso). When the isotonic loadwas changed to 50% Fiso, data points from the 20 and 50% Fiso experiments overlapped in thelength-Ca2+]i relationship. Similarly, datapoints from the 80% Fiso experiments clustered near thosefrom the 50% Fiso experiments. Therefore, despite 2.5- and4-fold differences in external load, Ca2+]idid not deviate much from the length-Ca2+]irelation that fitted the 20% Fiso data. Maximal inhibition of sarcoplasmic reticular (SR) Ca2+ uptake by 10 µMcyclopiazonic acid (CPA) did not significantly changeCa2+]i in carbachol-induced isometriccontractions and isotonic shortening. CPA also did not significantlychange myosin light-chain phosphorylation or force redevelopment whencarbachol-activated muscle strips were quickly released from optimallength (Lo) to 0.5 Lo. These results are consistent with thehypothesis and suggest that SR Ca2+ uptake is not theunderlying mechanism. |
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