Ai Fukumitsu1, Yukio Takano1,*, Ayako Iki1,
Kenji Honda1, Ryo Saito1, Takeshi Katsuragi2
and Hiro-o Kamiya1
1Department of Pharmacology, Faculty of Pharmaceutical Sciences, and 2Department of Pharmacology, School of Medicine,
Fukuoka University, Fukuoka 814 - 0180, Japan
* To whom correspondence should be addressed.
Abstract: Electrical field stimulation (EFS) caused contraction of isolated tail arteries of rats. The EFS-induced contraction showed frequency-dependence and was entirely abolished by the sodium channel blocker tetrodotoxin (1~10-7 M). The EFS-induced (at 20 Hz) contraction was reduced by about 60% in the presence of phentolamine (1~10-6 M). Therefore, later experiments were carried out in the presence
of phentolamine. Pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) (1~10-8 - 1~10-6 M) and basilen blue E-3G (3~10-5 - 5~10-5 M), P2-receptor antagonists, significantly inhibited the contraction evoked by EFS. In addition, PPADS significantly inhibited the contractions induced by ATP (1~
10-4 M) and a selective P2x-receptor agonist, ¿,À-methylene ATP (1~10-6 M). In contrast, basilen blue E-3G did not inhibit ¿,À-methylene ATP-induced contraction. The ecto-ATPase activator apyrase (5 and 10 U/ml) significantly reduced the EFS-induced contractions. These findings suggest that endogenous ATP released by EFS causes contractions of rat tail artery via both the P2x-receptors and P2y-receptors.
Keywords: P2x-receptor, P2y-receptor, Tail artery, ATP, Vasocontraction