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, α,β-methylene
ATP (1×10-6 M). In contrast, basilen blue E-3G did not inhibit
α,β-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