Possible physiological role of endogenous adenosine in defecation in rats.

Evacuated feces after intraperitoneal administration of selective adenosine receptor antagonists were evaluated in rats. The selective adenosine A1 receptor antagonists, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (100-300 micrograms/kg i.p.) and (R)-7,8-dihydro-8-ethyl-2-(3-noradamantyl)-4-propyl-1H-imidazo[2,1 -i]purin- 5(4H)-one (KF20274) (30-300 micrograms/kg i.p.), significantly increased defecation, whereas the selective adenosine A2 receptor antagonist 4-amino-8-chloro-1-phenyl[1,2,4]triazolo[4,3-a]quinoxaline (CP-66,713) failed to cause a significant increase at up to 10 mg/kg i.p. The defecation caused by DPCPX (100 micrograms/kg) was markedly alleviated by (2S)-N6-(2-endo-norbornyl)adenosine ((S)-ENBA) (30-300 micrograms/kg s.c.), a selective adenosine A1 receptor agonist, but not influenced by 2-[p-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosin e (CGS 21680) (30-1000 micrograms/kg s.c.), a selective adenosine A2 receptor agonist. These results suggest that endogenous adenosine plays a physiological role in sustained inhibition of defecation via adenosine A1 receptors.