ABSTRACT
The treatment with α1-adrenoceptor antagonists of the benign prostatic hyperplasia (BPH) symptom complex associated with obstruction of the lower urinary tract has evolved substantially from the original observations of Caine with phenoxybenzamine. Initially, only two types of α-adrenoceptor (α1 and α2) were identified. Phenoxybenzamine, an antagonist at both α-adrenoceptors, was classified as a nonselective α-adrenoceptor antagonist. Subsequently, the prime determinant of periurethral smooth muscle tone was found to be the α1-adrenoceptor, which led to the clinical evaluation of the first α1-selective antagonist, prazosin, in an attempt to improve the sideeffect profile of phenoxybenzamine. Understanding has increased further, to an extent where three major subtypes of the α1-adrenoceptor have been cloned and characterized, namely α1A, α1B, and α1D. A fourth receptor subtype, the α1Ladrenoceptor, has also been defined pharmacologically, but neither fully characterized nor cloned.1 The evolution of the nomenclature, which has been confusing and has undergone change over the last few years, is described in a review by Bylund et al.2
