Fernandez D, Snedden W, Fernandez P G, Nath C, Vasdev S, Triggle C R, Lee C
Division of Anatomic Pathology, Faculty of Medicine, Memorial University Medical School, St John's, Newfoundland.
Can J Cardiol. 1988 Jan-Feb;4(1):44-8.
The interaction of blood pressure, salt intake and the inhibition of angiotensin converting enzyme activity with cardiac hypertrophy were examined in the Dahl rat model. Eight-week-old salt sensitive and salt resistant rats were each separated into two colonies, one of which was maintained on a low salt and the other on a high salt diet for three weeks, at the end of which time both salt sensitive colonies were hypertensive. Each colony was then separated into two groups, one received no medication the other was given lisinopril until normotension was achieved. After 11 weeks of therapy, intra-arterial blood pressures and heart rates were recorded. The rats were sacrificed and heart weight to body weight ratios were determined. Both untreated salt sensitive groups displayed marked cardiac hypertrophy which correlated well with diastolic blood pressure irrespective of salt intake. Lisinopril therapy lowered blood pressures to normotensive levels in all groups except for salt sensitive rats ingesting a high salt diet where, despite a 10-fold increase in drug dose, normotension was not achieved. Significant cardiac regression accompanied lisinopril therapy in rats receiving low salt diets but high salt intake severely attenuated regression in both strains. There was no significant correlation between heart weight and blood pressure in the treated groups. The results suggest that cardiac regression appears to be mediated by other factors besides ventricular afterload pressure and that high salt intake adversely affects blood pressure and heart weight response to lisinopril therapy.
在Dahl大鼠模型中，研究了血压、盐摄入量以及血管紧张素转换酶活性抑制与心脏肥大之间的相互作用。将8周龄的盐敏感大鼠和盐抵抗大鼠各分为两个群体，其中一个群体维持低盐饮食，另一个群体维持高盐饮食3周，在这3周结束时，两个盐敏感群体均出现高血压。然后将每个群体再分为两组，一组不接受药物治疗，另一组给予赖诺普利直至血压恢复正常。治疗11周后，记录动脉内血压和心率。处死大鼠并测定心脏重量与体重之比。两个未治疗的盐敏感组均表现出明显的心脏肥大，且无论盐摄入量如何，均与舒张压密切相关。赖诺普利治疗使所有组的血压降至正常水平，但摄入高盐饮食的盐敏感大鼠除外，尽管药物剂量增加了10倍，仍未达到正常血压。接受低盐饮食的大鼠在赖诺普利治疗后出现明显的心脏逆转，但高盐摄入严重削弱了两个品系的逆转。治疗组中心脏重量与血压之间无显著相关性。结果表明，心脏逆转似乎是由心室后负荷压力以外的其他因素介导的，高盐摄入对赖诺普利治疗的血压和心脏重量反应产生不利影响。
