Renal hemodynamics of hypertensive patients are characterized by an increased renal vascular resistance (RVR), resulting in low renal plasma flow (RPF). Normal glomerular filtration rate (GFR) is maintained through an increased filtration fraction (FF). This pattern may have long term harmful consequences for the kidneys. Propranolol, given in the short- or long-term, lowers both RPF and GFR. Pindolol, as well as so called cardioselective beta-blockers and labetalol, alter renal hemodynamics only slightly, if not at all. In some studies, nadolol has been shown to increase RPF, leaving GFR unchanged. A new beta-blocker, tertatolol, seems to consistently increase RPF and GFR. These different renal actions of various beta-blockers are poorly explained. They may be, however, of clinical significance, in the short term for patients with already impaired renal function, and possibly over the long term for other hypertensive patients.