Abstract
The activity of Na+/K+ ATPase is a crucial factor in lots of functions of vascular and nonvascular smooth muscles. However, its role in muscle contractility of human prostate has not been well elucidated. In this context, we have examined the effect of ouabain on the contractile response and noradrenaline release in human prostate to clarify the role of cardiac glycoside in the pathophysiology of bladder outlet obstruction associated by benign prostatic enlargement. Human prostatic tissues (n = 12) were obtained at operation from males by open prostatectomy (n = 2) or transurethral resection of the prostate (n = 10). The effect of ouabain on muscle contraction and [3H]noradrenaline release was studied in human prostatic tissue. The action mechanism following the administration of ouabain was also examined. Ouabain concentration-dependently induced a gradual contraction in human prostate and this delayed contraction was significantly blocked by prazosin other than the other receptor antagonists. In parallel experiments, ouabain also caused a concentration-dependent gradual increase in [3H]noradrenaline release, which was extracellular Ca2+-dependent. Furthermore, ouabain-induced [3H]noradrenaline release increased, in a concentration-dependent manner, with increasing Na+ concentrations from 25 to 140 mM. Moreover, K+-free Krebs solution could mimic the [3H]noradrenaline release action to ouabain. Ouabain may induce an increase in tension response in human prostate, and this effect is due mainly to an increase in noradrenaline release via an effect on the Na+-dependent Ca2+ influx system.
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