Lantelme P, Cerutti C, Lo M, Paultre C Z, Ducher M
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.
Am J Physiol. 1998 Sep;275(3):R920-5. doi: 10.1152/ajpregu.1998.275.3.R920.
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.
1）比较里昂遗传性高血压（LH）大鼠、正常血压（LN）大鼠和低血压（LL）大鼠的自发性压力反射敏感性（SBRS）；2）评估LH大鼠压力反射受损机制的某些方面。在早期用培哚普利进行慢性转换酶抑制后，对对照动物进行压力反射研究，并在培哚普利治疗的大鼠中进行4周的血管紧张素II输注后进行研究。使用先前验证的方法，利用自由活动动物记录的血压（BP）和心率值之间的统计相关性来确定SBRS。LH大鼠表现出高血压、心脏肥大和SBRS降低（LH，1.3±0.2；LN，2.5±0.4；LL，2.2±0.4次·分钟-1·mmHg-1）。培哚普利可预防高血压和心脏肥大的发展，并使SBRS恢复正常。在输注血管紧张素II后，LH和LL大鼠的血压升高，但只有出现心脏肥大的LH大鼠的SBRS受损（LH，1.1±0.2；LN，2.5±0.2；LL，2.8±0.3次·分钟-1·mmHg-1）。用氯沙坦急性阻断血管紧张素II可部分逆转这种损害。这些结果表明，高血压并不能解释LH大鼠SBRS降低的原因。SBRS受损可能是由于心脏肥大或血管紧张素II对压力反射环的直接作用所致。
