Hemodynamic and renin responses to nifedipinein renovascular hypertension

Abstract

We investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics in twelve patients who had severe hypertension (diastolic values averaging 114 mm Hg) with unilateral renal artery stenosis (angiography) and hyperreninemia. Plasma renin activity was determined from blood samples drawn from the aorta and from both renal veins, so that "ischemic lateralization" could be evaluated through appropriately derived indexes. Nifedipine promptly and significantly lowered aortic pressure in all patients. At 30 minutes maximal circulatory responses were recorded, which consisted of a 22% decrease in mean aortic pressure (from an average of 144.6 +/- 15 mm Hg to an average of 113 +/- 11 mm Hg), a 44% reduction of systemic vascular resistance (from 2162 +/- 540 dynes.sec.cm-5 to to 1205 +/- 279 dynes.sec.cm-5), a 33% rise in cardiac index (from 2920 +/- 970 ml/min/m2 to 3875 +/- 986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 minutes of continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in persons with primary hypertension with similar levels of blood pressure. After nifedipine was given, renin activity of the systemic blood rose significantly, because of a potentiated release from the kidney with arterial stenosis. This effect, which was inferred as being due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)