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), NG-monomethyl-L-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.
|Number of pages||6|
|Journal||European Journal of Pharmacology: Environmental Toxicology and|
|Publication status||Published - 1995 Mar 16|
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