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Arterial hypertension contributes to the development of lipid abnormalities, as may also do so some antihypertensive drugs. Chronic hypercholesterolemia (HC) accelerates the atherosclerotic process, which in turn alters the vascular response to a variety of vasoactive agonists. Because of the cholesterol-membrane fluidity-ionic transport relationships, it is reasonable to propose that HC of short duration, unaccompanied by vascular morphologic changes, could first, alter vascular reactivity, and second, lead to early functional hemodynamic abnormalities. To answer these two questions, the following study was undertaken. HC was induced by feeding New Zealand rabbits a cholesterol (4%) and cholic acid (1%) enriched diet. The response to angiotensin II (10(-11) to 10(-8) M), of desendothelialized strips of aorta (A), mesenteric artery (MA) and vein (MV) obtained from rabbits fed during 1, 2, and 3 consecutive weeks, was examined using the cascade superfusion technique. HC fails to alter the aortic contractile response to angiotensin II. However, the MA contraction decreases by 48, 52, and 74% below baseline values (p < 0.01) after 1, 2, and 3 of HC. In contrast, the MV contraction is enhanced by 85, 87, and 22% above control values (p < 0.01) during the same periods of HC. In these animals, renal plasma flow (para-amino-hippurate clearance) decreased from 14.6 to 11.4, 8.8, and 9.3 ml/min (p < 0.01) after 1, 2, and 3 weeks of HC, while glomerular filtration rate (inulin clearance) similarly declined from 4.3 to 3.7 (NS), 2, 3, and 2.5 ml/min (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)