Carvedilol and the kidney

Antihypertensive drugs have differing effects on renal hemodynamics, tubular function, plasma electrolytes, and hormonal responses. Nonselective -blockers without intrinsic sympathomimetic activites, such as propranolol, have been reported to reduce renal blood flow and to cause a modest decrease in glomerular filtration rate. Carvedilol is a new multiple action agent displaying nonselective -blockade without intrinsic sympathicomimetic activity, ₁-adrenoceptor blockade (probably responsible for its vasodilator activity), and possibly also calcium antagonist properties. The presence of these different pharmacodynamic properties results in a different effect on the kidney as compared with, e.g., propranolol. In the dog, intrarenal infusion of carvedilol resulted in a renal vasodilator response with preservation of renal blood flow and without inducing sodium retention; in contrast, propranolol induced a renal vasoconstrictor response and sodium retention in this model. A renal vasodilator response to carvedilol was also reported in spontaneously hypertensive rats (SHR) and in DOCA-salt SHR. In contrast to labetalol, i.v. infusion of hypotensive doses of carvedilol in conscious SHR did not cause sodium retention. Carvedilol was effective in controlling hypertension and preserving renal function in a rat model of progressive hypertensive renal disease. In patients with essential hypertension, carvedilol was reported to reduce renal vascular resistance in the presence of reduced perfusion pressure, allowing for normal renal autoregulation of renal blood flow. Although a small reduction in glomerular filtration rate was seen after acute administration, renal function was preserved during chronic treatment. It is concluded from these studies that renal perfusion and renal function are well maintained during acute and chronic treatment with carvedilol. The compound does not appear to cause sodium retention, and preliminary animal test data suggest the possibility of a renoprotective effect.