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Development of hypertension, myocardial hypertrophy and the cardiac antioxidant status of male Dahl salt-sensitive (DSS) genetically hypertensive rats was evaluated and compared to that of normotensive Dahl salt-resistant (DSR) controls. In order to obtain exaggerated and more severe hypertension, half of the animals (10 per group) were Na loaded (8% NaCl diet) for 6 weeks. The myocardial antioxidant status was estimated in tissue homogenates on the basis of tissue glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The results showed that 6 weeks of hypertension resulted in left ventricle myocardial hypertrophy, documented by weight, morphometry and morphological changes. The compromised myocardial antioxidant status of the DSS rats was defined by significantly decreased GSH-Px and glutathione activity (13% and 41%, respectively) as compared to DSR rats. SOD in DSS myocardium was increased by 47% compared to that in DSR myocardium, an effect that is considered a compensatory mechanism to the oxidative stress. All of the above changes were exaggerated by NaCl loading. It was concluded that DSS rats, on either a normal or high NaCl diet, displayed decreased antioxidant capacity, which is most likely genetically determined. Before the Dahl rat can be considered as a suitable model for testing new cardiac antioxidants, a full characterization of the level of cardiac oxygen free radicals is required.
Somova et al. (Mon,) studied this question.