The effects of antihypertensive therapy on renal function.

Renal vascular resistance is increased in essential hypertension, with a consequent reduction in renal plasma flow together with a normal or slightly reduced glomerular filtration rate. Non-specific vasodilators may exacerbate this effect while loop diuretics, beta-blockers, angiotensin converting enzyme inhibitors and calcium antagonists may increase these renal hemodynamic parameters. We studied the effect of lacidipine, a new long-lasting calcium antagonist, on renal hemodynamics in 11 essential hypertensives. Lacidipine (4 mg once a day) acutely increased renal plasma flow without affecting the glomerular filtration rate. A transient, but non-significant, diuresis and natriuresis occurred. After 4 weeks of lacidipine treatment, all the parameters of renal function returned to basal levels. These results suggest that the well known renal effects of calcium antagonists are, at least in part, related to the onset of the antihypertensive effect being more pronounced with compounds such as nifedipine which have a rapid-onset, blood pressure-lowering effect.

In-vivo activation of circulating inactive renin by the ischemic kidney in man.

The role of the kidney as a possible source or as activator of inactive renin was studied in 22 patients with Essential Hypertension (EH) and in 20 patients with Unilateral Renal Artery Stenosis (RAS). Active and inactive renin (trypsin activation) were measured in blood samples taken simultaneously from both renal veins and from a peripheral artery during acute diuretic stimulation induced by furosemide 40 mg i.v. In EH pts active and trypsin-activated renin were significantly higher in both renal veins than in arterial blood (P less than 0.001 and P less than 0.02 respectively) whereas no difference was seen as far as inactive renin is concerned. In unilateral RAS trypsin-activated and active renin from the ischemic kidney were significantly higher (P less than 0.01 and P less than 0.005 respectively) while inactive renin was significantly lower (P less than 0.005) than in arterial blood. No significant difference was seen between arterial and renal venous blood from the contralateral kidney as far as active and inactive renin are concerned. When comparing the V-A differences for active renin to the corresponding V-A differences for inactive renin from the ischemic kidney a significant negative correlation appeared (r = -0.49 p less than 0.05) whereas no correlation was found from the contralateral kidney (r = -0.26 n.s.). These data demonstrate that the ischemic kidney, in addition to its ability to release active renin, can also activate circulating inactive renin.