The urinary bladder is a smooth muscle organ whose function is to collect and store urine at low intravesical pressures, and then to periodically expel the urine via a highly coordinated sustained contraction. Classically, the control of bladder function is through the autonomic nervous system. During bladder filling (at least in animal models), the sympathetic nervous system is active and this produces an increase in tension of the bladder base and urethra via activation of alpha-adrenergic receptors; and the relaxation of the bladder body via activation of beta-adrenergic receptors. In addition, sympathetic activity inhibits parasympathetic ganglionic transmission via postsynaptic sympathetic fibers which act upon alpha-2 type receptors located in the ganglion. Bladder emptying is mediated via the parasympathetic system with the activation of primarily muscarinic cholinergic receptors (and purinergic receptors in various animal species). In general, bladder function is dependent on the state of the neuronal innervation, the structure of the organ as a whole, the contractile response of the smooth muscle elements. Experimentally, an alteration in one factor will induce substantial adaptive changes in the other two. In this review, we will present some current concepts of urophysiology, uropharmacology, and uropathology; and how some of this current information may be helpful in the development of specific pharmacological agents directed specifically at the urogenital system.