Dietary-sodium-induced cardiac remodeling in spontaneously hypertensive rat versus Wistar–Kyoto rat

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Abstract
To study the effects of short-term and long-term high sodium intake on cardiac mass and design in sodium-sensitive spontaneously hypertensive rats versus sodium-resistant Wistar–Kyoto rats. Young spontaneously hypertensive rats and Wistar–Kyoto rats were randomly allocated to control diet, 2 or 8% dietary sodium for 2–12 weeks and changes in resting hemodynamics, cardiac angiotensin II level, sympathetic activity and cardiac structure evaluated. Sympathetic activity was assessed by measuring levels of plasma catecholamines, responses of blood pressure to ganglionic blockade, and rates of cardiac turnover of norepinephrine. High sodium intake for 4 weeks increased left ventricle weight of Wistar–Kyoto rats aged 4 weeks (by 11 and 25% for 2 and 8% NaCl diets, respectively). This hypertrophic response was temporary, however, had already diminished after 6 weeks, and was absent after 12 weeks of a high sodium intake. However, after prolonged exposure concentric remodeling occurred (i.e. left ventricle wall thickness: radius ratio increased with no change in left ventricle mass). High sodium intake did not affect resting blood pressure, cardiac index, cardiac angiotensin II level, and general sympathetic activity of Wistar–Kyoto rats. Short-term high sodium intake did not increase left ventricle mass of young spontaneously hypertensive rats, unless sodium intake was so high (8% NaCl) that blood pressure and general sympathetic activity increased, too. However, a prolonged moderate (2%) increase in sodium intake also caused concentric remodeling in spontaneously hypertensive rats without increasing left ventricle mass, blood pressure, cardiac index, and general and cardiac sympathetic activities. The blood pressure in young Wistar–Kyoto rats is sodium-insensitive but the heart structure is sodium-sensitive and high dietary sodium intake causes an early hypertrophic response, and then concentric remodeling. In contrast, hypertrophic response appears to occur after the response of blood pressure in spontaneously hypertensive rats, whereas the remodeling is similar to that in Wistar–Kyoto rats.