Mechanics of K(+)-induced isotonic and isometric contractions in isolated canine coronary microarteries

P. J. Boels, V. A. Claes and D. L. Brutsaert Department of Physiology and Medicine, University of Antwerp, Belgium. The effects of shortening in isotonic contractions on the mechanics of microvascular smooth muscle were investigated. Intramyocardial canine coronary microarteries (in situ diameter 60 +/- 3 microns) were mounted as rings, connected to a newly developed photoelectromagnetic force-length transducer, and activated with 125 mM K+. Shortening during isotonic contractions depressed the length-force relation (shortening deactivation) compared with the length-force relation obtained from isometric contractions; the effect was present at the earliest moments after activation, suggesting that a fundamental mechanism associated with the actual sliding of contractile filaments delayed onset of contractile activity in isotonic contractions compared with isometric contractions. Force-velocity relations were obtained by isotonic quick releases from isotonic and isometric contractions at various times. Isotonic shortening before the quick releases reduced the constants of the apparent hyperbolic force-velocity relations and maximal velocity of shortening (Vmax) compared with isometric contractions released at the same time. Increasing contraction duration reduced Vmax but more so in isotonic than in isometric contractions. Vmax also decreased with decreasing instantaneous length. A possible effect of force development on Vmax before the isotonic quick release was also described. Quick increments of load during isotonic contractions were sustained during active shortening in the phasic part, but during the tonic part loading resulted in a pronounced transient relaxation. Thus, in microvascular preparations, active isotonic shortening altered the length-force, force-velocity, and velocity-time relations and uncovered a time-dependent sensitivity to loading conditions. These experiments suggested that the mechanics of smooth muscle contraction may contribute significantly to the mechanisms of the physiological control of coronary microvascular diameter.