ABSTRACT
The two major components of lower urinary tract symptoms (LUTS)—voiding (obstructive) and storage (irritative) symptoms-associated with benign prostatic hyperplasia (BPH) have traditionally been linked directly or indirectly to pathophysiologic changes in the prostate.1
Voiding symptoms have been attributed to two facets of prostate function: the physical mass of the enlarged gland (the static component) and the tone of the smooth muscle of the prostate stroma (the dynamic component).2 Storage symptoms, however, have been more closely associated with the bladder dysfunction produced secondary to the increased outflow resistance, arising from prostate-dependent urethral obstruction. The precise interrelationship between morphologic BPH, bladder outflow obstruction, and profile of
