[Circulatory and renin response to the administration of nifedipine in renovascular hypertension].

In 12 severe (diastolic values averaging 114 mmHg) hypertensives with unilateral renal artery stenosis (angiography) and hyperreninemia, we investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics. Plasma renin activity was determined on blood samples withdrawn from the aorta and both renal veins, so that "ischemic lateralization" could be evaluated through appropriated derived indexes. Nifedipine promptly and significantly lowered the aortic pressure in all patients. At 30 min maximal circulatory responses were recorded, which consisted of 22% decrease in mean aortic pressure (from an average of 144.6 +/- 15 to an average of 113 +/- 11 mm Hg), 44% reduction of systemic vascular resistance (from 2162 +/- 540 to 1205 +/- 279 dynes.S.cm-5), 33% rise of cardiac index (from 2920 +/- 970 to 3875 +/- 986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 min continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in primary hypertensives with similar levels of blood pressure. After nifedipine, renin activity of the systemic blood significantly rose, due to a potentiated release from the kidney with arterial stenosis. This effect, that was interfered as a 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 of cases. It is suggested that nifedipine may not only be regarded as an additional diagnostic tool, but also as an effective antihypertensive agent in this disorder, al least in the short term. This contrasts with the previous suggestion of nifedipine as substantially more effective in low-renin rather than high-renin hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)