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Am J Physiol Regul Integr Comp Physiol 275: R920-R925, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 3, R920-R925, September 1998

Mechanisms of spontaneous baroreflex impairment in Lyon hypertensive rats

Pierre Lantelme, Catherine Cerutti, Ming Lo, Christian Z. Paultre, and Michel Ducher

Département de Physiologie et Pharmacologie Clinique, Centre National de la Recherche Scientifique Unité Propre de Recherche de l'Enseignement Supérieur Associée 5014, Faculté de Pharmacie, 69008 Lyon, France

This experiment aimed at 1) comparing the spontaneous baroreflex sensitivity (SBRS) in Lyon genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) rats and 2) assessing some aspects of the mechanisms of its impairment in LH rats. Baroreflex was studied in control animals after an early chronic converting enzyme inhibition with perindopril and after a 4-wk infusion of ANG II in perindopril-treated rats. The SBRS was determined with a previously validated method, using statistical dependence between blood pressure (BP) and heart rate values recorded in freely moving animals. LH rats exhibited high BP, cardiac hypertrophy, and decreased SBRS (LH, 1.3 ± 0.2; LN, 2.5 ± 0.4; LL, 2.2 ± 0.4 beats · min-1 · mmHg-1). Perindopril prevented the development of hypertension and cardiac hypertrophy and normalized SBRS. BP rose in LH and LL rats after ANG II infusion, but only LH rats, which developed a cardiac hypertrophy, had an impaired SBRS (LH, 1.1 ± 0.2; LN, 2.5 ± 0.2; LL, 2.8 ± 0.3 beats · min-1 · mmHg-1). This impairment was partially reversed by an acute ANG II blockade with losartan. These results demonstrate that high BP does not account for the decreased SBRS in LH rats. SBRS impairment could result either from cardiac hypertrophy or from the direct effect of ANG II on the baroreflex loop.

renin-angiotensin system; cardiac hypertrophy; statistical dependence


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