Physiological and pathological regulation of the autonomic control of urinary bladder contractility.

The urinary bladder stores urine for most of the day, a process facilitated by beta-adrenergic receptor-mediated detrusor relaxation and alpha(1)-adrenergic receptor-mediated contraction of the bladder neck. Physiological voiding is caused by detrusor contraction induced by muscarinic receptor stimulation. This manuscript reviews data on alterations of alpha(1)- and beta-adrenergic and of muscarinic responsiveness of the detrusor related to gender, developmental maturation, ageing and pathophysiological conditions such as diabetes, arterial hypertension and bladder outlet obstruction, all of which can be associated with alterations of bladder function such as bladder overactivity. The existing data show that none of the conditions associated with bladder overactivity exhibit increased muscarinic receptor responsiveness which could explain the clinical observations; while not being fully consistent, they if anything show a reduced responsiveness. On the other hand, more limited data demonstrate that alpha(1)-adrenergic responsiveness may be enhanced and beta-adrenergic responsiveness reduced in states associated with bladder overactivity. However, the existing data are too sparse and/or too inconsistent to allow definitive conclusions. Thus, alterations distinct from those of autonomic receptors may be better candidates to explain bladder dysfunction.