In vivo assessment of the contribution of [alpha]b1- or [bêta]- adrenoceptor stimulation in the development of dietary sodium-induced cardiac hypertrophy in rats.

Abstract

Hypothesis. High sodium diet in rats may induce intermittent sympathetic activation through increasing nighttime water intake, and may enhance cardiac adrenergic responses via an increase in adrenoceptor activity, which may contribute to the development of high sodium diet-induced left ventricular hypertrophy (LVH). Method. In conscious WKY rats, resting hemodynamics and after blocking baroreflex by hexamethonium (Hex), hemodynamic responses to $\alpha\sb1$-, or $\beta$-agonist (phenylephrine, Phe, or isoproterenol, Iso), and then ventricular weights and LV dimensions were determined after 1, 2, 4 or 6 wk medium high or high sodium diet (2 or 8% NaCl) with or without ig administration of $\alpha\sb1$- or $\beta$-blockers (60 $mg/kg/day$ terazosin, Tz, 25 or 100 $mg/kg/day$ nadolol, Nd, alone or both Tz and Nd). Discussion. High sodium diet for 2 to 6 wk induces concentric LVH, without changing most resting hemodynamics including LV filling pressures. Vasodilatation by $\beta$-agonist was attenuated and negative chronotropy of $\alpha\sb1$-agonist augmented by a longer salt exposure, which may indicate a decreased vascular $\beta\sb2$- or an increased sinoatrial node $\alpha\sb1$-receptor responses. Effects of ganglionic and adrenergic blockades suggest a salt-augmented sympathetic control on peripheral arterial resistance. Chronic $\alpha\sb1$- and/or $\beta$-blockers failed to prevent the high sodium diet-induced LVH, which suggests that adrenoceptor activation does not play a primary role in evoking this LVH. However, the blockers shifted the LVH from a concentric to an eccentric form, and Tz augmented the salt-increased water intake. It is plausible that a volume overload-induced hypertrophy associated with the blockers may have masked a reduction in the high sodium diet-induced LVH. (Abstract shortened by UMI.)