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Eur Respir J 2003; 22:227-234
Copyright ©ERS Journals Ltd 2003

Mechanics and crossbridge kinetics of tracheal smooth muscle in two inbred rat strains

F-X. Blanc1,2, C. Coirault1,3, S. Salmeron1,2, D. Chemla1,3 and Y. Lecarpentier1,3

1 INSERM LOA ENSTA, Polytechnic School, Palaiseau, 2 Pneumology Unit, Dept of Internal Medicine, and 3 Dept of Cardiovascular and Respiratory Physiology, Bicêtre Hospital, University of Paris XI, Assistance Publique, Hôpitaux de Paris, Le Kremlin-Bicêtre, France

CORRESPONDENCE: F-X. Blanc, Unité de Pneumologie, Service de Médecine Interne, Centre Hospitalier Universitaire de Bicêtre, 78, rue du Général Leclerc, 94275 Le Kremlin-Bicêtre, France. Fax: 33 145212632. E-mail: xavier.blanc@bct.ap-hop-paris.fr

Keywords: airways, crossbridge, hyperresponsiveness, myosin, smooth muscle

Received: July 17, 2002
Accepted March 25, 2003

S. Salmeron was the recipient of a grant from CNRS and AP-HP (Praticien de Recherche Associé).

The aim of the study was to determine whether the nonspecific in vivo airway hyperresponsiveness of the inbred Fisher F-344 rat strain was associated with differences in the intrinsic contractile properties of tracheal smooth muscle (TSM) when compared with Lewis rats.

Isotonic and isometric contractile properties of isolated TSM from Fisher and Lewis rats (each n=10) were investigated, and myosin crossbridge (CB) number, force and kinetics in both strains were calculated using Huxley's equations adapted to nonsarcomeric muscles. Maximum unloaded shortening velocity and maximum extent of muscle shortening were higher in Fisher than in Lewis rats (~46% and ~42%, respectively), whereas peak isometric tension was similar.

The curvature of the hyperbolic force/velocity relationship did not differ between strains. Myosin CB number and unitary force were similar in both strains. The duration of CB detachment and attachment was shorter in Fisher than in Lewis rats (~–46% and –34%, respectively).

In Fisher rats, these results show that inherited, genetically determined factors of airway hyperresponsiveness are associated with changes in crossbridge kinetics, contributing to an increased tracheal smooth muscle shortening capacity and velocity.




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