Relaxation of rat thoracic aorta induced by pyridine

• Published in: European journal of pharmacology 1995-03, Vol.292 (3), p.265-270
• Main Authors: Hsu, Kuei-Sen, Lin-Shiau, Shoei-Yn
• Format: Article
• Language: English
• Subjects: Animals; Aorta, Thoracic - drug effects; Aorta, Thoracic - metabolism; Biological and medical sciences; Ca 2+ influx; Caffeine - pharmacology; Calcium - metabolism; Cyclic AMP - metabolism; Cyclic GMP - metabolism; Endothelium, Vascular - physiology; Female; In Vitro Techniques; Male; Medical sciences; Miscellaneous; Muscle Relaxation - drug effects; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; Norepinephrine - antagonists & inhibitors; Norepinephrine - pharmacology; Pharmacology. Drug treatments; Potassium - antagonists & inhibitors; Potassium - pharmacology; Pyridine; Pyridines - pharmacology; Rats; Rats, Wistar; Vasorelaxation
• ISSN: 0926-6917; 0014-2999
• DOI: 10.1016/0926-6917(95)90031-4

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), N G - monomethyl- L-arginine acetate (50 μM) or methylene blue (50 μM). In high-K + medium (80 mM), pyridine inhibited the Ca 2+ concentration-dependent vasocontraction. Moreover, in Ca 2+-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 45Ca 2+ 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 Ca 2+ channel-blocking properties in vascular smooth muscle.