Vasodilators, antihypertensive therapy, and the kidney

Abstract

Whether or not the kidney is involved in the genesis of hypertension in an individual patient, it becomes a major determinant of the response to antihypertensive therapy once a treatment strategy is adopted. The major mechanisms through which the kidney influences blood pressure are renin release and sodium retention, either together or separately, but additional mechanisms may also contribute. When sodium intake is restricted or a diuretic is used, the reactive increase in plasma renin activity makes a substantial contribution to limiting the decrease in blood pressure. When vasodilators or agents that block the sympathetic nervous system are used, sodium retention plays an important role. Among newer agents, the effectiveness of calcium-channel blockers, converting-enzyme inhibitors, and perhaps dopamine analogs reflects, for reasons that differ from one class of agent to another, a special action on the kidney that limits the reactive renal response to the reduction in blood pressure. Treatment strategies that address the problem of the renal response are more likely to be effective than approaches that avoid or ignore it.