Relaxation of rat thoracic aorta induced by pyridine

Abstract

The pharmacological and toxicological activity of pyridine was determined in rat thoracic aorta. Pyridine inhibited norepinephrine (3 μM)-induced phasic and tonic contractions in the thoracic aorta as well as the endothelium-denuded aorta of the rat. The tonic pre-contraction elicited by norepinephrine was also relaxed by the addition of pyridine and this relaxing effect was not affected by indomethacin (20 μM), $\text{N}{}^{\mathrm{<mtext>G</mtext>}}\text{-}\text{monomethyl-}\text{L}\text{-arginine acetate}$ (50 μM) or methylene blue (50 μM). In high-K⁺ medium (80 mM), pyridine inhibited the Ca²⁺ concentration-dependent vasocontraction. Moreover, in Ca²⁺-free medium, the norepinephrine (3 μM)-induced phasic contraction was also suppressed by pyridine, while the caffeine (10 mM)-induced contraction remained unaffected. The cAMP and cGMP levels of rat aorta were not changed by pyridine. The ⁴⁵Ca²⁺ influx elicited by either norepinephrine or high-K⁺ was inhibited by pyridine in a concentration-dependent manner. All of these findings indicated that pyridine relaxes rat thoracic aorta by virtue of its Ca²⁺ channel-blocking properties in vascular smooth muscle.