The response of autonomic receptors to castration and testosterone in the urinary bladder of the rabbit.

The effects of castration and testosterone on the autonomic receptor density and contractility in the urinary bladder smooth muscle of male rabbits were compared to untreated animals. Four groups of rabbits were studied over a similar time span with Group 1 animals serving as the untreated controls. Two groups (Groups 2 and 3) were castrated 28 days prior to sacrifice, Group 2 animals received corn oil for 14 days, and Group 3 animals received testosterone, 10 mg./day, for 14 days. The Group 4 animals were non-operated and received testosterone 10 mg./day for 14 days. Ligand saturation binding studies for alpha adrenoceptors in the bladder base and proximal urethra were performed with [3H]dihydroergocryptine ([3H]DHE). Muscarinic cholinergic receptors (MChR) were assayed with [3H]quinuclidinyl benzilate ([3H]QNB) and beta adrenoceptors with [125I]iodocyanopindolol ([125I]CYP) on the detrusor smooth muscle. Castrated Group 2 animals showed no significant change in receptor density with either [3H]QNB or [125I]CYP in detrusor muscle, but did exhibit a significant reduction (59%) of alpha adrenoceptors in the bladder base-urethra. The testosterone treated castrate and testosterone treated non-operated animals had significant increases in the MChR density, but no change in the alpha adrenergic, or beta adrenergic receptor density as compared to untreated controls. Cumulative dose response contractile studies were performed with carbachol on detrusor muscle strips and with phenylephrine on bladder base strips in isolated organ baths. The contractile studies on muscles from Groups 1, 2 and 3 showed no change in the ED50 or maximal contractile strength between control, castration or testosterone treated castrated animals. The ratio of wet bladder weight as compared to total body weight between each of the treatment groups showed a slight increase in both of the testosterone treatment groups. It was concluded that castration down regulates the alpha adrenergic receptors of the bladder base, while testosterone treatment increases the density of MChRs, and increases the ratio of the bladder to total body weight. Although no contractile changes were observed in the bladder base tissue it is conceivable that longer chronic testosterone deficits might ultimately affect the bladder outlet resistance in the male because of the reduced alpha adrenergic receptor density.