Lack of endothelial dysfunction in the young genetically hyperlipidemic JCR:LA-cp rat

V. Hampl, S. L. Archer, J. C. Russell, D. P. Nelson, E. K. Weir

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Hyperlipidemia impairs endothelium-derived relaxing factor (EDRF) in systemic vessels. To test the hypothesis that the pulmonary circulation is less prone to such impairment, we compared isolated lungs, pulmonary artery rings, and aortic rings of hereditary hyperlipidemic JCR:LA-cp/cp (corpulent) rats with their genetically relevant controls, JCR:LA+/+ (lean) rats at the age of 2.5 months. The JCR rats were also compared with Sprague-Dawley rats of the same age. Endothelium-dependent pulmonary vasodilation in response to acetylcholine, bradykinin, L-arginine, and calcium ionophore A23187, as well as pulmonary vasoconstriction to angiotensin II, acute hypoxia, KCl, norepinephrine, and phenylephrine, differed little between lean and corpulent rats. However, unexpectedly, endothelium-dependent vasodilation was not impaired even in the aortic rings at this age. The Sprague-Dawley rats responded considerably more than either group of JCR rats to nitroprusside, angiotensin II, acute hypoxia, KCl, and norepinephrine. We conclude that, in contrast to other models of hypercholesterolemia, endothelium-dependent vasodilation is not impaired in 2.5-month-old hyperlipidemic JCR:LA-cp rats. Pulmonary vasoconstriction and vasodilation is greater in Sprague-Dawley than in JCR:LA-cp rats.

Original languageEnglish (US)
Pages (from-to)186-195
Number of pages10
JournalJournal of Vascular Medicine and Biology
Issue number4
StatePublished - 1993


  • JCR:LA-cp rat
  • Pulmonary vascular reactivity
  • endothelium
  • endothelium-derived relaxing factor
  • hyperlipidemia


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