A novel classification of α‐₁ adrenoceptor subtypes (High, Low) was applied to human benign prostatic hypertrophy (BPH)tissue.

Human BPH specimens were examined by a radioligand binding assay method using ³H‐prazosin, and those data were compared with preoperative therapies.

(1) Scatchard analysis showed a high‐affinity site (K_d:27.18 ± 6.41 pM; B_max:9.29 ± 0.98 fM/mg protein; mean ± SE) as α_1H, and a low‐affinity site (K_d:4088.0 ± 744.34 pM; B_max:140.81 ± 19.98 fM/mg protein; mean ± SE) as α_1L subtype, for prazosin. (2) The K_d and B_max were not different in the nontreated group (n = 5), α₁ blocker group (n = 5), and antiandrogen group (n = 5), in either α₁‐high affinity or α₁‐low affinity subtype. (3) Phenoxbenzamine had different pK_i value for the above two adrenoceptor subtypes. Scatchard analysis showed that α₁‐high affinity binding site disappeared in the presence of 1 μM of phenoxbenzamine, and the K_d and B_max values in the prescence of 1 μM of phenoxybenzamine were almost identical to the α₁‐low affinity site of the two subtypes.

Human BPH tissue possesses both α_1H‐and α_1L‐adrenoceptor subtypes according to the affinities for prazosin, and only the α_1H subtype can be completely inhibited by some concentration of phenoxybenzamine. Treatent by α₁ blocker may not change the conditons of α₁‐adrenoceptors in prostatic tissue.Prostate 31:216–222, 1997. © 1997 Wiley‐Liss, Inc.