Adjustable passive length-tension curve in rabbit detrusor smooth muscle

Abstract

Until the 1990s, the passive and active length-tension (L-T) relationships of smooth muscle were believed to be static, with a single passive force value and a single maximum active force value for each muscle length. However, recent studies have demonstrated that the active L-T relationship in airway smooth muscle is dynamic and adapts to length changes over a period of time. Furthermore, our prior work showed that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that in addition to viscoelastic behavior, DSM displays strain-softening behavior characterized by a loss of passive stiffness at shorter lengths following a stretch to a new longer length. This loss of passive stiffness appears to be irreversible when the muscle is not producing active force and during submaximal activation but is reversible on full muscle activation, which indicates that the stiffness component of passive force lost to strain softening is adjustable in DSM. The present study demonstrates that the passive L-T curve for DSM is not static and can shift along the length axis as a function of strain history and activation history. This study also demonstrates that adjustable passive stiffness (APS) can modulate total force (35% increase) for a given muscle length, while active force remains relatively unchanged (4% increase). This finding suggests that the structures responsible for APS act in parallel with the contractile apparatus, and the results are used to further justify the configuration of modeling elements within our previously proposed mechanical model for APS.

Altered hemodynamics, endothelial function, and protein expression occur with aortic coarctation and persist after repair

“…Vascular rings (width: 3-4 mm) were sectioned, cleaned of adhering perivascular tissue, mounted on an isometric myograph (Harvard Apparatus, Holliston, MA), maintained in a water-jacketed tissue bath in PSS bubbled continuously with O2 at 37°C, and allowed to equilibrate for at least 1 h. An optimal resting force of 2 g was applied to all sections based on preliminary experiments with this model (43,58). Arteries underwent K ϩ -PSS contraction followed by three PSS rinses, and this procedure was conducted two to three times until the effective force response of an artery was consistent (27,59). To quantify endothelial function, aortic rings were subsequently precontracted with 0.2 M phenylephrine (PE), and endothelium-dependent NO relaxation was determined by cumulative additions of ACh (10 Ϫ9 -10 Ϫ5 M) (3,4).…”

Evidence that actomyosin cross bridges contribute to “passive” tension in detrusor smooth muscle

“…DSM activation at short muscle lengths by KCl, a muscarinic receptor agonist and a prostaglandin receptor agonist, regenerates APS and thus passive tension at longer muscle lengths via a rhoA kinase (ROCK)-dependent mechanism (1,46). Therefore, ROCK activation appears to add a dynamic passive tension component (i.e., APS) in parallel with a static passive tension component presumably due to extracellular matrix proteins (47).…”

Mechanics of Vascular Smooth Muscle

“…26B, dashed parabolic active stress-strain curve). Adjustable preload stress is weakened by strain and moves rightward with loading (i.e., the effect of loading is to cause strain softening, and the "lost" stress is identified as adjustable preload stress) (382,442,447). This rightward movement continues until the preload stress becomes dominated at long muscle lengths by the acutely stationary passive stress.…”