The chronic use of propranolol is characterized by 10%-20% decrements of renal plasma flow (RPF) and glomerular filtration rate (GFR). The results of most investigations, however, suggest that the use of nadolol, a long-acting nonselective agent, spares renal function. Similarly, intrinsic sympathomimetic activity (ISA)-positive and cardioselective beta-adrenergic inhibitors and the combined alpha-beta blocker, labetalol, appear to preserve renal hemodynamics. The reason(s) for the apparent disparate effects of various beta blockers is uncertain. The pathophysiological mechanisms are probably multifactorial and relate to either diminished cardiac output or increased renal vascular resistance, or both. It is possible that inhibition of renal vasodilator mechanisms plays a role. The explanation for the relative absence of adverse effects with a given medication probably varies from agent to agent. The clinical implications of beta-blocker-induced renal changes are presently unknown. The alterations are probably not clinically important in patients with normal renal function. In patients with underlying renal insufficiency, there is no reason to avoid the use of beta-adrenoceptor blockers. In some patients, however, one may wish to prescribe those beta blockers that tend to spare RPF and GFR.