Vasodilators, antihypertensive therapy and the kidney

Both traditional and newer treatments of essential hypertension are discussed in relation to kidney function and renal perfusion. In essential hypertension, renal vascular resistance is routinely increased and renal blood flow is often decreased. Reduced sodium intake as a form of therapy will cause a decrease in both renal blood flow and glomerular filtration, most likely due to an angiotensin-induced renal vasoconstriction caused by the reactive increase in renin release. Treatment with diuretics produces the same effects, also angiotensin-mediated. The addition of a beta-adrenergic blocking agent to prevent renin release may be a good choice, but individual agents within this class must be examined for direct renal vasoconstriction. The effects of "nonspecific" vasodilators on renal perfusion and renal sodium handling vary with the patient but may produce antinatriuresis, sodium retention and decrease in glomerular filtration. Studies with calcium antagonists have shown promising results. Nifedipine studies show a substantial increase in renal plasma flow, a well-maintained glomerular filtration rate and a brisk diuresis and natriuresis. However, patients with the lowest baseline renal flow do not show these benefits. Diltiazem has shown a potentiated renal vascular response in normotensive patients of hypertensive parents. Angiotensin converting enzyme inhibitors such as captopril and enalapril have produced increased renal blood flow and well-maintained glomerular filtration in patients with essential hypertension. The agents available for treating hypertension have improved dramatically in the past decade. A salutary effect on the kidney will remain high on the list of important characteristics to be considered in choosing one of these agents.