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SUMMARY Twenty-six essential hypertensive patients were entered into a protocol to assess the blood pressure and renal effects of the dihydropyridine calcium antagonist nifedipine (30-120 mg/day given in divided doses) administered for 4 weeks. Nifedipine monotherapy effectively lowered blood pressure in 73% of the patients. Glomerular filtration rate and effective renal plasma flow were increased 13.3 and 19.6%, respectively. The filtration fraction and urinary albumin excretion remained unchanged. Renal vascular resistance was markedly reduced (25.2%). Changes observed in renal function were independent of the patients' initial glomerular filtration rate. 1 ' 2 The potential role for calcium antagonists to reverse or prevent the pathophysiological progression of hypertensive renal disease or to attenuate the progression of chronic renal disease is unknown.We have previously reported on the renal effects of the benzothiazepine calcium antagonist diltiazem 3 * and the dihydropyridine calcium antagonist amlodipine.3 These studies suggested that calcium antagonists have the potential to enhance effective renal plasma flow (ERPF) and renal blood flow, to preserve or Received August 24, 1987; accepted December 3, 1987. improve glomerular filtration rate (GFR), and to lower renal vascular resistance. We now report on the shortterm renal effects of the dihydropyridine calcium antagonist nifedipine. Our results suggest that renal function abnormalities encountered in the essential hypertensive state may be improved by nifedipine independently of its systemic blood pressure effect.Patients and Methods Twenty-six patients with essential hypertension were selected for this prospective study. To be included, each patient had to maintain a mean 5-minute recumbent diastolic blood pressure (fifth phase) between 95 and 114 mm Hg following withdrawal of prior drug therapy and during 2 to 4 weeks of placebo therapy. The diagnosis of essential hypertension was established by history and physical examination and by the absence of clinical findings suggestive of a secondary form of hypertension. Excluded from the study were patients with a history or clinical or laboratory findings of moderate to severe cardiomegaly, congestive heart failure, recent myocardial infarction, second-or thirddegree heart block, overt diabetes mellitus, or Grade 3 or 4 Keith-Wagener hypertensive retinopathy, as well as patients who were nonadherent to drug therapy (as monitored by count of returned tablets).

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This study examined the relationship between right atrial pressure (RAP), urine flow rate, sodium excretion rate, and plasma atrial natriuretic peptide (ANP) levels after an acute Ringer expansion. Two groups of rats had their RAP monitored and balloon catheters placed in their thoracic inferior venae cavae. In one group the balloon remained deflated, and in the second group the balloon was inflated during the volume expansion in an attempt to prevent the rise in RAP. The peak RAP was 7.3 +/- 0.8 mmHg when the balloon remained deflated and 3.5 +/- 0.6 mmHg in the group with the balloon catheter inflated (P less than 0.005). The corresponding peak ANP levels were 682 +/- 140 and 223 +/- 40 pg/ml. There was a significant correlation between the peak RAP and ANP levels (r = 0.754; P less than 0.05). The inflation of the balloon catheter significantly decreased the urine flow rate and the urine sodium excretion rate. A final group of animals had 200 microliters of rabbit serum containing antibody to ANP infused before the volume expansion. The antibody-treated animals had significantly lower urine flow and sodium excretion rates than nonantibody-treated control rats. We conclude that ANP is one of the factors which allows the rat to excrete an acute Ringer expansion.

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