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慢性L-精氨酸甲酯(L-NAME)治疗诱导的左心室肥厚的消退:卡托普利的作用

Regression of chronic L -NAME-treatment-induced left ventricular hypertrophy: effect of captopril.

作者信息

Bernátová I, Pechánová O, Pelouch V, Simko F

机构信息

Institute of Normal and Pathological Physiology, Comenius University, Bratislava, Slovak Republic.

出版信息

J Mol Cell Cardiol. 2000 Feb;32(2):177-85. doi: 10.1006/jmcc.1999.1071.

DOI:10.1006/jmcc.1999.1071
PMID:10722795
Abstract

Long-term administration of N(G)-nitro- L -arginine methyl ester (L -NAME) induces development of NO-deficient hypertension and left ventricular (LV) hypertrophy. In this work, we examined the effect of spontaneous and captopril-induced recovery on LV hypertrophy and protein composition in rats with developed L -NAME-induced hypertension. Four groups of rats were investigated: control L -NAME 40 mg/kg/day for 4 weeks (L -NAME) L -NAME 40 mg/kg/day for 4 weeks followed by 3-week spontaneous recovery (L -NAME+R) L -NAME 40 mg/kg/day for 4 weeks followed by 3 weeks of captopril treatment at a dose of 100 mg/kg/day (L -NAME+C). LV hypertrophy in the L -NAME group was associated with an increase in content and concentration of left ventricular DNA and RNA, concentration of metabolic proteins (MP) and soluble collagenous proteins (SCP). Spontaneous recovery period reduced the hypertension, without regression of LV hypertrophy. Left ventricular DNA and RNA content were increased in the L -NAME+R group. In this group, concentrations of MP, contractile proteins (CP), and collagenous proteins did not differ from those in the L -NAME group. Captopril treatment caused total regression of hypertension and LV hypertrophy and decreased both content and concentration of DNA and RNA, as well as the contents of MP, CP and SCP v the L -NAME group. However, after captopril treatment, concentration of collagenous and non-collagenous protein fractions remained increased v control. We conclude that spontaneous regression of L -NAME-induced hypertension is not associated with regression of LV hypertrophy. LV hypertrophy was regressed only in captopril-treated animals.

摘要

长期给予N(G)-硝基-L-精氨酸甲酯(L-NAME)可诱发一氧化氮缺乏型高血压和左心室(LV)肥厚。在本研究中,我们检测了自发性恢复和卡托普利诱导恢复对已发生L-NAME诱导型高血压大鼠左心室肥厚和蛋白质组成的影响。研究了四组大鼠:对照组;L-NAME 40 mg/kg/天,持续4周(L-NAME组);L-NAME 40 mg/kg/天,持续4周,随后自发性恢复3周(L-NAME+R组);L-NAME 40 mg/kg/天,持续4周,随后以100 mg/kg/天的剂量给予卡托普利治疗3周(L-NAME+C组)。L-NAME组的左心室肥厚与左心室DNA和RNA含量及浓度增加、代谢蛋白(MP)和可溶性胶原蛋白(SCP)浓度增加有关。自发性恢复期降低了高血压,但左心室肥厚并未消退。L-NAME+R组左心室DNA和RNA含量增加。在该组中,MP、收缩蛋白(CP)和胶原蛋白的浓度与L-NAME组无差异。卡托普利治疗使高血压和左心室肥厚完全消退,并使DNA和RNA的含量及浓度以及MP、CP和SCP的含量均低于L-NAME组。然而,卡托普利治疗后,胶原蛋白和非胶原蛋白组分的浓度仍高于对照组。我们得出结论,L-NAME诱导型高血压的自发性消退与左心室肥厚的消退无关。只有在卡托普利治疗的动物中左心室肥厚才消退。

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