Bladder Smooth Muscle Contractility Research Articles

Alterations in the expression of the beta-cytoplasmic and the gamma-smooth muscle actins in hypertrophied urinary bladder smooth muscle.

The obstruction of the bladder outlet induces a marked increase in bladder mass, and this is accompanied by reduced contractility of bladder smooth muscle and alteration in the cellular architecture. In this study, we show that the composition of various isoforms of actin, a major component of the contractile apparatus and the cytoskeletal structure of smooth muscle, is altered in response to the obstruction-induced bladder hypertrophy. Northern blot analysis of the total RNA isolated from hypertrophied urinary bladder muscle, using a cDNA probe specific for smooth muscle gamma-actin, shows over 200% increase in the gamma-actin mRNA. However, the estimate of the amount of actin from the 2D gel reveals only a 16% increase in gamma-actin, since the 2D gel electrophoresis does not distinguish gamma-smooth muscle actin from gamma-cytoplasmic actin. The bladder smooth muscle alpha-actin and the smooth muscle alpha-actin mRNA are not altered in response to the hypertrophy. The obstructed bladder also reveals a decrease in the beta-cytoplasmic actin (37%) and a concomitant diminution in the beta-cytoplasmic actin mRNA (29%). Hence, the composition of the actin isoforms in bladder smooth muscle is altered in response to the obstruction-induced hypertrophy. This alteration of the actin isoforms is observed at both the protein and mRNA levels.

Dissociation of Relaxation and Myosin Light Chain Dephosphorylation in Porcine Uterine Muscle

Bladder outlet obstruction induces detrusor hypertrophy and it can eventually lead to decreased bladder smooth muscle contractility. Heat shock protein 20 is the proposed mediator of force suppression in vascular smooth muscle. We investigated whether heat shock protein 20 could also mediate the decreased contractility observed in partially obstructed rat bladders.Female Wistar rats (Harlan Laboratories, Indianapolis, Indiana) were randomized to partial urethral ligation or sham ligation. After 3 weeks the rats were sacrificed, and the bladders were harvested, frozen, homogenized and analyzed for heat shock protein 20 content by Western blot immunoreactivity. The content of myosin regulatory light chain, a constitutively expressed protein, was determined as a control. Bladder smooth muscle strips were dissected from some rats and mounted for force generation measurement.At cystectomy obstructed bladders were significantly heavier and had more residual urine compared to sham operated bladders. Heat shock protein 20 immunoreactivity was significantly increased a mean ± 1 SEM of 1.9 ± 0.3-fold in obstructed vs sham operated bladders. Control protein myosin regulatory light chain immunoreactivity did not significantly differ in obstructed and sham operated bladders. Maximal stress, that is force per cross-sectional area, was significantly decreased in obstructed vs sham operated bladders. Human bladder was found to express immunoreactive heat shock protein 20.We noted that partially obstructed rat bladders 1) express higher levels of heat shock protein 20 and 2) generate less stress than sham operated bladders. These data suggest the possibility that heat shock protein 20 over expression could at least partially mediate the decreased contractile activity observed with partial bladder outlet obstruction. The mechanism for increased heat shock protein 20 expression is unknown but it may involve increased mechanical stress or hypoxia from urethral obstruction. Human bladder expressed immunoreactive heat shock protein 20, suggesting that a similar mechanism could potentially occur in humans. If confirmed in humans, patients with clinical conditions that result in detrusor hypocontractility could potentially benefit from pharmacological interventions aimed at inhibiting heat shock protein 20.

Arg 8]vasopressin-induced contractions of rabbit urinary bladder smooth muscle

The effects of a number of neurohypophyseal hormones and analogues on the contractility of rabbit urinary bladder smooth muscle in vitro were examined. The order of potency was [Arg 8]vasopressin = [Lys 8]vasotocin > [Lys 8]vasopressin > [Arg 8]vasotocin ⪢ [deamino 1,D-Arg 8]vasopressin > oxytocin ⪢ pressinoic acid. The maximum tension induced by [Arg 8]vasopressin was 4.4 N·cm −2 and the pD 2 was 8.7. The effects of [Arg 8]vasopressin were competitively antagonized by [(β-mercapto-β,β-cyclopentamethylenepropionic acid) 1, (O-methyl)Tyr 2, Arg 8]vasopressin and by [deaminopenicillamine 1, Val 4, D-Arg 8]vasopressin with pA 2s of 8.4 and 6.6, respectively. It was concluded that rabbit urinary bladder smooth muscle contains receptors for the neurohypophyseal hormones which have recognition properties similar to V1-vasopressin receptors.

Modeling the contractility of urinary bladder smooth muscle using isometric contractions.

In the course of developing a clinical contractility index, isometric contractions of pig urinary bladder smooth muscle were analyzed in terms of phase plots (a plot of the rate of change of a variable, in this case force, as a function of the variable itself). The straight line describing the major part of the phase plots is characterized by the two parameters Fiso (the horizontal intercept) and c (the slope) of the line. It was found that changes in the geometry of the tissue sample and changes in extracellular calcium grossly influence Fiso, but not c, whereas changes in prestimulus rest time influence c, but not Fiso. It is concluded that Fiso is related to the number of available contractile units, and c is related to the limiting rate constant in the excitation-contraction coupling, which is probably determined by the release of intracellular calcium. The existence of the calcium paradox and the interpretation of the concept of facilitation or potentiation in this type of smooth muscle are discussed.