Effects of dietary sodium on cardiac responses to adrenergic stimulation in vitro.

Abstract

Objective. To evaluate the role of $\alpha\sb1$- or $\beta$-adrenoceptors in dietary sodium-induced cardiac hypertrophy, we assessed (1) the effects of high sodium diet (8% NaCl) on the responses of hearts isolated from young WKY rats to $\alpha\sb1$- or $\beta$-adrenergic stimulation after 1, 2, or 6 weeks of high sodium intake and (2) the effects of high sodium diet on responses of hearts isolated from young WKY rats after 2 weeks of high sodium intake to $\alpha\sb1$- or $\beta$-adrenoceptor subtype stimulation. Conclusions. Studies using methoxamine as an $\alpha\sb1$-agonist, as an $\alpha\rm\sb{1a}$-adrenoceptor agonist in the presence of CEC, or as an $\alpha\rm \sb{1b}$-adrenoceptor agonist in the presence of urapidil or the use of isoproterenol as a non-selective $\beta$-agonist revealed no significant differences in the sensitivity of ventricular $\alpha\sb1$-adrenoceptor subtypes or $\beta$-adrenoceptors between hearts from rats on a control or high sodium diet at any duration of feeding. A possible effect of high sodium diet on atrial $\alpha\rm \sb{1a}$- or $\alpha\rm \sb{1b}$-adrenoceptors is suggestive. The unchanged ventricular contractile responses to $\alpha\sb1$ or $\beta$-adrenoceptor stimulation in the hypertrophied hearts suggest that changes in ventricular adrenergic receptors responsiveness do not play a role in dietary sodium-induced left ventricular hypertrophy. One can not exclude a dissociation of intracellular signals linked to $\alpha\sb1$- or $\beta$-adrenoceptors associated with dietary sodium induced cardiac hypertrophy from those associated with contractility. (Abstract shortened by UMI.)