ACUTE HYPOTENSION/HYPERTENSION IN VITRO CAUSES TEMPORARY POST-RECEPTOR UP/DOWN REGULATION OF SUBSEQUENT ARTERIAL CONTRACTIONS

BEDNAREK M; MINER AS; ALVAREZ SM; SPEICH JE; RATZ PH

New Orleans, Louisiana

Congreso; Experimental Biology 2009 FASEB; 2009

American Phisiology Society and others

The amount of tension a striated muscle can generate in uniquely dependent on muscle length (i.e., length-tension curves are static). Early (1970’s) studies demonstrated that smooth muscle length-tension curves appeared also to be static, but recent evidence suggests that smooth muscle length-tension curves can be dynamic. In short, studies suggest that the degree of tension produced is a function of the duration the muscle remains at any particular length. Identification of the mechanism(s) permitting length-history adaptation should provide insights into vascular contractile pathophysiology. Using in vitro arterial rings (rabbit femoral artery), our goal was to characterize, and identify mechanisms causing length-history adaptation. Two contractions induced immediately after release from its optimum length for muscle contraction (Lo) to 0.8-fold Lo revealed incremental increases in active tension such that the 2 contraction was 0.13-fold that of the 1. If the muscle was stretched briefly from 0.8- to 1.2- and 1.4-fold Lo between the 1 and 2 contractions at 0.8-fold Lo, the 2 contraction was diminished in strength by, respectively, 0.12- and 0.60-fold the 1 contraction (i.e., it was down-regulated). A 3 contraction 1 hr later permitted near complete restoration of active tension. Preliminary data suggest that length-history adaptation was not caused by alterations in cell calcium nor myosin light chain phosphorylation, which lends support to the view that numbers of crossbridges rather than crossbridge regulation may play the predominant role in vascular smooth muscle length-history adaptation. Support: RO1HL061320.