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[Effect of hypercholesterolemia on vascular reactivity: repercussions on renal hemodynamics in the rabbit]
1Département de médecine, Faculté de médecine, université de Sherbrooke, Québec, Canada.
Insights
Chronic hypercholesterolemia (HC) alters vascular reactivity, decreasing mesenteric artery contraction and increasing vein contraction. This study investigated early hemodynamic changes in rabbits with short-term HC.
Area of Science:
- Cardiovascular Physiology
- Lipid Metabolism
- Vascular Biology
Context:
- Arterial hypertension and hypercholesterolemia (HC) contribute to atherosclerosis.
- Cholesterol's impact on cell membranes may alter vascular reactivity and hemodynamics.
- Early functional changes precede morphological alterations in vascular disease.
Purpose:
- To investigate the effects of short-term HC on vascular reactivity.
- To determine if HC induces early hemodynamic abnormalities.
- To assess changes in aortic, mesenteric artery, and vein responses to angiotensin II.
Summary:
- New Zealand rabbits were fed a cholesterol-enriched diet for 1-3 weeks to induce HC.
- Vascular strips (aorta, mesenteric artery, vein) and renal function were assessed.
- HC reduced mesenteric artery contraction and increased vein contraction, while aortic response was unchanged. Renal plasma flow and glomerular filtration rate decreased.
Impact:
- Short-term HC significantly alters vascular reactivity in a tissue-specific manner.
- Early functional hemodynamic changes occur before significant morphological vascular damage.
- Findings suggest HC directly impacts vascular smooth muscle and renal function, contributing to cardiovascular risk.
Abstract:
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)