The distribution of α‐ and β‐adrenoceptors in isolated preparations of human bladder neck and detrusor muscle has been studied. Adrenaline caused contraction of the bladder neck which was blocked by phenoxybenzamine but unaltered by propranolol. Isoprenaline caused relaxation of the bladder neck which was blocked by propranolol. High concentrations caused contraction which was enhanced by propranolol but blocked by phenoxybenzamine. Detrusor muscle was relaxed by isoprenaline and this effect was blocked by propranolol. Phenylephrine caused relaxation of detrusor which was unaffected by phenoxybenzamine; in some cases contraction was produced in the presence of propranolol. It is concluded that the bladder neck contains mainly α‐receptors and the detrusor mainly β‐receptors but both regions possess both types of adrenoceptor.

The serum paraoxon hydrolyzing activities in a Canadian population were bimodally distributed and interethnically variable. A clear separation between the two phenotypes was obtained by determining the ratio of activity in the presence of 5 × 10−3 M CaCl2 plus 5 × 10−1 M NaCl over that in 5 × 10−3 M CaCl2 alone. The data strongly suggest that the crucial discriminatory role was played by Ca2+.

In cumulative dose-response studies, strips from bladder neck of rabbit were significantly more sensitive to stimulation with noradrenaline, phenylephrine, and methoxamine than were strips from detrusor. There was no difference between the two regions in sensitivity to isoprenaline or carbachol. From the known characteristics of these agents, it seemed unlikely that metabolic destruction or uptake could account for the different sensitivities seen. Also, neither normetanephrine nor desmethylimipramine could alter significantly the potency of noradrenaline in either area of the bladder. It seems likely that the difference in sensitivity to alpha-adrenoceptor stimulation in the bladder neck and detrusor is due to factors at the receptor level.

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