Effects of Ba(2+) on norepinephrine-induced contraction of rat thoracic aorta in vitro

The aim of this study was to examine the effect of exogenously applied BaCl(2) on the norepinephrine-induced contraction of the rat thoracic aorta. Exogenously applied BaCl(2) (0.3-1 mmol/l) slightly elevated the norepinephrine-induced sustained contraction of the rat thoracic aorta in the absence of nicardipine (1 micromol/l). In the aortic preparation pretreated with nicardipine (1 micromol/l), exogenous BaCl(2) (0.1-3 mmol/l) did not elevate the norepinephrine-induced sustained contraction, but the high concentration of BaCl(2) (10 mmol/l) slightly inhibited the norepinephrine-induced tone. In a Ca(2+)-free Krebs bi- carbonate solution (KBS) containing norepinephrine (1 micromol/l) or a Ca(2+)-free K(+)-rich (60 mmol/l) KBS, exogenously applied BaCl(2) (1-30 mmol/l) caused a sustained contraction of the rat thoracic aorta, and this sustained contraction was completely inhibited by nicardipine (1 micromol/l). Exogenous CaCl(2) (0.1-3 mmol/l) also caused a sustained contraction of the aortic preparation in a Ca(2+)- free KBS containing norephinephrine (1 micromol/l), but such a sustained contraction was partly inhibited by nicardipine (3 micromol/l). These results indicate that Ba(2+) elevates the norepinephrine-induced tone of the rat isolated thoracic aorta by permeating voltage-dependent Ca(2+) channels in the absence of nicardipine, but that Ba(2+) has a minor modification on the norepinephrine-induced sustained contraction of the nicardipine-pretreated preparation.