Adaptation of the length-active tension relationship in rabbit detrusor

Abstract

Studies have shown that the length-tension (L-T) relationships in airway and vascular smooth muscles are dynamic and can adapt to length changes over a period of time. Our prior studies have shown that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that can shift along the length axis as a function of strain history and activation history. The present study demonstrates that the active L-T curve for DSM is also dynamic and that the peak active tension produced at a particular muscle length is a function of both strain and activation history. More specifically, this study reveals that the active L-T relationship, or curve, does not have a unique peak tension value with a single ascending and descending limb, but instead reveals that multiple ascending and descending limbs can be exhibited in the same DSM strip. This study also demonstrates that for DSM strips not stretched far enough to reveal a descending limb, the peak active tension produced by a maximal KCl-induced contraction at a short, passively slack muscle length of 3 mm was reduced by 58.6 +/- 4.1% (n = 15) following stretches to and contractions at threefold the original muscle length, 9 mm. Moreover, five subsequent contractions at the short muscle length displayed increasingly greater tension; active tension produced by the sixth contraction was 91.5 +/- 9.1% of that produced by the prestretch contraction at that length. Together, these findings indicate for the first time that DSM exhibits length adaptation, similar to vascular and airway smooth muscles. In addition, our findings demonstrate that preconditioning, APS and adaptation of the active L-T curve can each impact the maximum total tension observed at a particular DSM length.

Length Adaptation of the Passive-to-Active Tension Ratio in Rabbit Detrusor

“…3,[6][7][8]12,13,19,21,22 However, a model explaining how both L-T curves can shift simultaneously has not been developed because L-T a and L-T p curves are thought to be caused by structurally distinct molecules in spatially distinct locations. This study builds upon our recent work which identified adaptation of the L-T a relationship in bladder 24 and our previous work characterizing the L-T p relationship in bladder. [25][26][27] Our previous studies showed that the L-T p relationship in rabbit DSM is dynamic and that DSM exhibits adjustable passive stiffness characterized by an L-T p curve that can shift along the length axis as a function of strain history and activation history.…”

“…Together, our previous studies demonstrate that both APS and length adaptation of the L-T a curve each impact the maximum total tension observed at a particular DSM length. 24,26 What remains to be determined regarding the role of length adaptation on the L-T relationships in DSM includes (1) whether adaptation at one particular muscle length shifts the entire L-T a curve, as has been suggested to occur in ASM; 31 (2) whether adaptation from a longer to a shorter length is different from adaptation from a shorter to a longer length; and (3) the relationship between adaptation of the L-T a and L-T p curves. Answering these questions will provide important insight into the role of length adaptation in DSM.…”

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

“…Because muscle cell active tension is due to the transmission through cytoskeletal adhesion junctions of tension generated by actomyosin cross bridges, the proposed mechanisms for length adaptation of active tension include changes in actin and myosin polymerization leading to addition and subtraction of sarcomeres, and sarcomere and cytoskeletal adhesion junction reorganization (13,16,17,25). Although the most extensive work on length adaptation of active tension has been done on airway smooth muscle (12), there is also evidence of length adaptation of active tension in certain arteries (40,51), rabbit bladder (45), and cat ileum (3).…”

Cerebral Artery Remodeling in Rodent Models of Subarachnoid Hemorrhage

“…The concept that the tension-generating capacity of SMCs is a steep function of diameter has been acknowledged for many decades. The notion that this active strain-tension relation is malleable is well appreciated for airway and bladder SMCs [43,44,45], while recent work also demonstrates such plasticity in small arteries. We previously demonstrated contractile plasticity in mesenteric arteries exposed to flow restriction in vivo [11] or following overnight incubation with ET-1 [10].…”