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Nicorandil Stimulates Release Of Adenyl Purines From Porcine Coronary Artery
Author(s) -
Sasaki Tetsuya,
Hashimoto Michio,
Nosaka Seishi,
Hanada Tomoki,
Saitoh Yuhei,
Yamauchi Masanobu,
Nakayama Kengo,
Masumura Sumio,
Tamura Katsuhiro
Publication year - 2000
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2000.03319.x
Subject(s) - nicorandil , vasodilation , adenosine , artery , chemistry , medicine , isosorbide dinitrate , cromakalim , nitric oxide , purine , pharmacology , cardiology , biochemistry , enzyme , receptor , agonist
SUMMARY 1. To clarify the mechanism of the cardioprotective effect of nicorandil (2‐nicotinamidoethyl‐nitrate ester), the effects of nicorandil and nitric oxide (NO) donors on the release of ATP, ADP, AMP and adenosine from arterial segments and cultured endothelial cells of the porcine coronary artery were examined. 2. Nicorandil significantly increased the release of total adenyl purines from arterial segments and from cultured endothelial cells. 3. Cromakalim, an ATP‐sensitive K + channel opener, did not affect the release of total adenyl purines from coronary artery segments. 4. S ‐Nitroso‐ N ‐acetyl‐ D , L ‐penicillamine and isosorbide dinitrate, NO donors, significantly increased the release of total adenyl purines from coronary artery segments. 5. These results demonstrate that nicorandil stimulates ATP release from the coronary artery by acting not as an ATP‐sensitive K + channel opener, but as a nitrate, thus suggesting the cardioprotective properties of nicorandil.