Role of Blood Pressure in the Natriuretic Response to Acute Calcium Channel Blockade in Humans

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Abstract
Summary: Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and renal excretion of sodium and lithium were measured before and after acute oral administration of 20 mg nifedipine in 19 essential hypertensive patients. In 10 of them, with a diastolic pressure <105 mm Hg, nifedipine resulted in a decrease in mean blood pressure toward normal (109 × 2 to 97 × 2, p < 0.001), a 27% increase in ERPF (p < 0.001), no change in GFR, and an increase in fractional sodium excretion (28%, p < 0.001). In nine subjects with a diastolic pressure 105 mm Hg, nifedipine produced a decrease in mean blood pressure (13 × 6 to 117 × 4, p < 0.001), which however remained higher than in mild hypertensives (p < 0.001). ERPF rose by 29% (p < 0.001), GFR remained unchanged, and fractional sodium excretion definitely increased more than in mild hypertensives (126%, p < 0.001), as did fractional lithium excretion, used as an estimate of proximal tubular sodium handling. Acute nifedipine produces renal vasodilation in hypertensives, but with a greater natriuretic response in those subjects whose blood pressure remains elevated. Thus, acute natriuresis following nifedipine administration is largely dependent on the interaction between changes in arterial pressure and renal hemodynamics.

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