Renal effects of beta-adrenoreceptor blockade

Abstract

Beta-adrenoreceptor blockers do not substantially alter renal function as measured by blood urea nitrogen, serum creatinine, or endogenous creatinine clearance. But there is evidence that insulin clearance may be decreased even when creatinine clearance is apparently normal, suggesting that the latter parameter may not dependably measure GFR during beta blockade, perhaps due to increased tubular creatinine secretion. A reduction in renal blood flow also can occur, but this is not a consistent finding and does not appear to correlate with changes in renal function. Unlike most other nondiuretic antihypertensive agents, beta blockers do not normally cause sodium and water retention. Thus, measurable increases in plasma volume do not occur even with long-term treatment, and body weight appears to increase only when the beta blockers are superimposed upon preexisting diuretic treatment. The most demonstrable intrarenal effect of the majority of beta blockers is their suppression of renin release, which in turn decreases production of AII and aldosterone. Inhibition of the mineralocorticoid hormone aldosterone may be a key factor in minimizing volume retention during treatment, whereas decreases in the peripheral vasoconstrictor actions of AII might play a part in the antihypertensive effects of these agents.