EFFECTS OF NICORANDIL AND ITS CONGENERS ON MUSCULATURE AND VASCULATURE OF THE DOG TRACHEA INSITU

  • 1 January 1982
    • journal article
    • research article
    • Vol. 258  (2) , 260-266
Abstract
In anesthetized dogs, the tracheal vascular bed in situ was perfused with arterial blood through the cannulated cranial thyroid arteries. The effects of nicorandil, a coronary vasodilator, and its congeners (SG-212 [N-(2-bromoethyl)nicotinamide hydrochloride], SG-209 [N-(2-acetoxyethyl)nicotinamide] and SG-103 [N-(2-nicotinoyloxyethyl)nicotinamide hydrochloride], in which the nitroxy group of nicorandil was substituted for other groups) on the tracheal musculature and vasculature were examined. All drugs were injected intraarterially. Nicorandil (10-300 .mu.g), SG-212 (100 .mu.g to 3 mg), SG-209 (100 .mu.g to 3 mg) and SG-103 (100 .mu.g to 3 mg) all produced a decrease in tracheal tone elevated by neostigmine (tracheal dilatation) and an increase in tracheal blood flow (tracheal vasodilatation). Relative potencies of these effects were, in descending order, nicorandil > SG-212 = SG-209 = SG-103 in producing tracheal dilatation, and nicorandil > SG-209 > SG-212 > SG-103 in producing tracheal vasodilatation. Nicorandil could also be a potential bronchodilator. The nitrate site in nicorandil apparently plays a role in potentiating the pharmacological activity of congeners of nicorandil.

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