Alpha1-receptors, when activated, generally cause smooth muscle contraction, so blocking these would not promote detrusor muscle relaxation and increased bladder storage. Instead, it could exacerbate the patient's symptoms.

Alpha2-receptors are primarily presynaptic and their activation inhibits release of norepinephrine, reducing sympathetic outflow. Blocking these receptors increases norepinephrine release, which doesn't typically lead to smooth muscle relaxation of the detrusor muscle.

Beta1-receptors are mainly found in the heart, and their activation increases heart rate and contractility. Blocking these receptors would not directly affect the detrusor muscle of the urinary bladder.

Beta2-receptors are found primarily in the lungs, GI tract, liver, uterus, vascular smooth muscle, and skeletal muscle. When stimulated, they generally cause smooth muscle relaxation, which in the urinary tract leads to increased bladder storage capacity. Therefore, agents that block the action of endogenous catecholamines (i.e., norepinephrine) on beta2-receptors would help alleviate symptoms related to urinary frequency, urgency, and nocturia.