Biochemical aspects of salt-induced, pressure-independent left ventricular hypertrophy in rats.

In an attempt to investigate the effect of chronic salt loading on heart size and biochemical composition, sixty 3-month-old male Wistar-Kyoto rats (WKY) were equally divided into two groups: One group was given 1% NaCl in drinking water, and the other group was given tap water as the control. After 7 months, five randomly selected rats from each group were examined for body weight (BW), indirect blood pressure (BP), hematocrit (Hct), and organ weights. Ventricles of the heart, aorta, and mesenteric arteries were biochemically analyzed for collagen (C) and noncollagenous protein NC) and deoxyribonucleic acid (DNA). Although here was no difference between the salt and control groups in BP (129 +/- 3 mmHg vs. 125 +/- 4 mmHg, mean +/- SE), BW (376 +/- 8 g vs. 372 +/- 5 g) and Hct (42.8% +/- 1.0% vs. 44.3% +/- 0.8%), left ventricular weight (857 +/- 19 mg vs. 788 +/- 8 mg) and kidney weight (2.59 +/- 00.9 g vs 2.31 +/- 0.05 g) were both significantly (P less than 0.01) greater in the salt group, whereas the weights of the right ventricle, aorta, and adrenal glands were equal. Biochemical analysis showed significant increase in NC/DNA ratio and total collagen content as well as decreased DNA concentration in the left ventricle of the salt group compared with the control, suggesting hypertrophy rather than hyperplasia of myocardial cells with concomitant activation of collagen synthesis. Since the manner of reactive collagen production appeared different from that reported for spontaneously hypertrophic rats (SHR) or in hypoxia- or aortic constriction-induced cardiac hypertrophy, some unique mechanism may be involved in salt-induced cardiac hypertrophy.