Search

To test the tolerance to nitrendipine in arterial hypertension secondary to chronic renal parenchymatous disease, a group of 10 patients so diagnosed and adequately controlled with a diuretic alone or with a beta-blocker were switched to nitrendipine at a dose to insure similarly adequate control of blood pressure. Patients were followed for 1 year at monthly intervals during which blood pressure measurement and the determination of a biochemical profile were performed. During the follow-up, nitrendipine adequately controlled blood pressure and a significant fall was observed in hematocrit (p less than 0.05) and serum uric acid (p less than 0.01) values. Meanwhile, the glomerular filtration rate, determined by the creatinine clearance, did not exhibit significant changes nor did the 24-h urinary excretion of proteins. The tolerance of the drug was adequate, with two patients presenting minimal ankle edema. These results seem to indicate that nitrendipine can be safely used in patients with arterial hypertension secondary to chronic renal parenchymatous disease.

The hypothesis that pregnancy induced hypertension (PIH) is associated with abnormal physiological control of plasma renin activity (PRA) was tested by studying the effects of graded infusion of angiotensin II (ANG II) on PRA, plasma aldosterone (PA), and blood pressure in normal pregnancy, PIH, non-pregnant women in luteal and follicular phase of the menstrual cycle, and males. PIH occurring in the second trimester was associated with elevated PRA, PA and blood pressure compared with all other groups, and reduced urinary thromboxane excretion compared with normal pregnancy. Exogenous ANG II infusion failed to suppress existing PRA in patients with PIH, in contrast to all other groups, but increased PA in all groups. It is concluded that PIH occurring in the second trimester is associated with elevated PRA, PA and blood pressure. The inability of circulating ANG II to reduce PRA in PIH may constitute a major alteration underlying the pathophysiology of PIH.

To evaluate the renal effects of nisoldipine (N), a dihydropyridine derivative, we have evaluated the variations of blood pressure (BP), heart rate, glomerular filtration rate (GFR), renal plasma flow (RPF), 24-h natriuresis, and renal capacity to excrete an i.v. sodium load (2,000 ml isotonic saline in 4-h) in response to a 4-day course of therapy with placebo (P) and N in six normotensive volunteers and six mild-to-moderate essential hypertensive patients. Both volunteers and patients were studied on two constant diets (20 and 150 mEq of sodium daily). No parameters changed after P. On the contrary, N induced a significant fall of BP (p less than 0.01) in the group of patients but not in volunteers. In both groups RPF and GFR increased significantly (p less than 0.05-0.01) while on a low sodium intake but remained constant when sodium intake was high. In the two groups studied, nisoldipine exhibited natriuretic properties manifested by an increase in the 24-h output of sodium as well as by an increased renal capacity to excrete the i.v. sodium load. These natriuretic properties were present in both situations of sodium load and could be facilitated by the change in renal hemodynamics observed when the intake of sodium was low.

In order to elucidate whether or not the natriuretic properties of calcium entry blockers persist during the long-term administration of the drug, we have investigated the renal capacity to excrete an intravenous sodium load (2,000 ml of isotonic saline in 4 h) in a group of eight mild to moderate essential hypertensive patients, before and after 1, 8, and 24 weeks of treatment with nitrendipine. The following parameters were measured before and hourly during saline infusion: blood pressure, and plasma and urine sodium and potassium. For 5 days prior to the performance of the test, the patients received a diet containing 120 mEq of sodium daily. Nitrendipine induced a significant fall of both systolic and diastolic blood pressure (p less than 0.05-0.01) that was maintained throughout the study. A significant increase of the cumulative renal sodium output (microEq/min/h) was observed after 1, 8, and 24 weeks (p less than 0.05-0.001) of therapy with the calcium entry blocker. Meanwhile, plasma sodium and potassium and the kaliuresis did not change significantly. These results indicate that the natriuretic effect of calcium entry blockers is still present after long-term treatment.

We studied the long-term effect of an angiotensin converting enzyme (ACE) inhibitor, captopril, on the progression of chronic renal failure and on the rate of urinary protein excretion. When compared with standard triple therapy, captopril slowed the progression of renal failure. Captopril was also able to reduce the proteinuria of non-diabetic glomerular origin. This reduction was not dependent on the presence or absence of arterial hypertension but was limited by the presence of low serum albumin levels, and only occurred in patients with proteinuria in excess of 3 g/24 h.