Effects of Ba2+ on Norepinephrine-Induced Contraction of Rat Thoracic Aorta in vitro

Abstract

The aim of this study was to examine the effect of exogenously applied BaCl₂ on the norepinephrine-induced contraction of the rat thoracic aorta. Exogenously applied BaCl₂ (0.3–1 mmol/l) slightly elevated the norepinephrine-induced sustained contraction of the rat thoracic aorta in the absence of nicardipine (1 μmol/l). In the aortic preparation pretreated with nicardipine (1 μmol/l), exogenous BaCl₂ (0.1–3 mmol/l) did not elevate the norepinephrine-induced sustained contraction, but the high concentration of BaCl₂ (10 mmol/l) slightly inhibited the norepinephrine-induced tone. In a Ca²⁺-free Krebs bi- carbonate solution (KBS) containing norepinephrine (1 μmol/l) or a Ca²⁺-free K⁺-rich (60 mmol/l) KBS, exogenously applied BaCl₂ (1–30 mmol/l) caused a sustained contraction of the rat thoracic aorta, and this sustained contraction was completely inhibited by nicardipine (1 μmol/l). Exogenous CaCl₂ (0.1–3 mmol/l) also caused a sustained contraction of the aortic preparation in a Ca²⁺- free KBS containing norephinephrine (1 μmol/l), but such a sustained contraction was partly inhibited by nicardipine (3 μmol/l). These results indicate that Ba²⁺ elevates the norepinephrine-induced tone of the rat isolated thoracic aorta by permeating voltage-dependent Ca²⁺ channels in the absence of nicardipine, but that Ba²⁺ has a minor modification on the norepinephrine-induced sustained contraction of the nicardipine-pretreated preparation.