Cardiac hypertrophy and cardiac renin-angiotensin system in Dahl rats on high salt intake

Objective On high salt intake, Dahl salt-sensitive rats develop cardiac hyp ertrophy disproportionate to the degree of hypertension. In the present stu dies, we assessed whether the cardiac hypertrophy induced by high salt depe nds on the development of hypertension per se, and leads to over-activity o f the cardiac renin-angiotensin system (RAS), Methods Cardiac angiotensin converting enzyme (ACE) mRNA and activity, card iac and plasma angiotensin I and II (AngI, II), as well as plasma renin act ivity (PRA) were assessed in Dahl salt-sensitive (Dahl S) and salt-resistan t (Dahl R) rats on high (1370 mu mol/g food) or regular salt (120 mu mol/g food) diet for 2-5 weeks, Cardiac ACE and hypertrophic response in Dahl S o n high salt were also assessed after central blockade of sympathetic hypera ctivity and hypertension. Results In Dahl S rats, ACE mRNA and activity of the left ventricle (LV) in creased markedly after 4-5 weeks of high salt diet compared with Dahl S on the central diet and Dahl R on either diet, Chronic intra-cerebroventricula r treatment with Fab fragments blocking brain 'ouabain' prevented the hyper tension by high salt in Dahl S rats but did not affect the salt-induced inc reases in LV weight or in LV ACE mRNA and activity. On regular salt diet, D ahl S rats demonstrated significantly lower cardiac AngI and AngII than Dah l R rats. However, high salt intake did not cause significant changes in ca rdiac AngI and II in either strain, On regular salt diet, PRA, plasma AngI and II were all significantly lower in Dahl S versus R, in Dahl S rats, hig h salt did not cause further decreases of the already low PRA or plasma Ang I and II. Conclusions These data indicate a low activity of both circulatory and card iac RAS in Dahl S versus R rats, The marked cardiac hypertrophy and increas e in cardiac ACE mRNA and activity induced by high salt in Dahl S do not de pend on the increase in blood pressure, High salt intake did not increase c ardiac AngII in Dahl S, suggesting that the increase in ACE mRNA and activi ty may be relevant for non-angiotensinergic mechanisms involved in cardiac hypertrophy, J Hypertens 2000, 18:1319-1326 (C) Lippincott Williams & Wilki ns.