Adrenergic blocking agents and the kidney

The acute and chronic renal effects of the beta-adrenergic antagonists, alpha 1-adrenergic antagonists, central alpha 2-adrenergic agonists, and central and/or peripheral adrenergic-neuronal blocking agents are reviewed. In general, beta-adrenergic antagonists have little or no clinical effect on glomerular filtration rate (GFR), effective renal plasma flow or renal blood flow (ERPF/RBF), renal vascular resistance (RVR), urinary sodium or potassium excretion, free water clearance, or body fluid composition. The alpha 1-adrenergic antagonists (prazosin and indoramin) have little or no clinical effect on GFR and ERPF/RBF; however, RVR is reduced. Sodium excretion is also reduced, leading to salt and water retention. The central alpha 2-adrenergic agonists (alpha-methyldopa, clonidine, and guanabenz) have little or no clinical effect on GFR and ERPF/RBF; however, RVR is reduced. Urinary sodium and potassium excretion and body fluid composition are unchanged. Free water clearance may be increased. The central and peripheral adrenergic-neuronal blocking agent reserpine has little or no clinical effect on GFR and ERPF/RBF; however, RVR is reduced. Urinary sodium, potassium, and water excretion and body fluid composition are unchanged. Finally, the peripheral adrenergic-neuronal blocking agents (guanadrel and guanethidine) decrease GFR and ERPF/RBF; RVR is also reduced. The filtered load and fractional excretion of sodium is decreased, producing expansion of body fluid spaces and weight gain.