Mizumoto H, Karasawa A
Department of Pharmacology, Kyowa Hakko Kogyo Co., Ltd., Shizuoka, Japan.
Jpn J Pharmacol. 1993 Oct;63(2):257-9. doi: 10.1254/jjp.63.257.
Effects of an adenosine A1-receptor agonist and antagonist were determined in pertussis toxin (IAP)-treated and non-treated rats. (-)-N6-(2-phenylisopropyl) adenosine, an adenosine A1-agonist, reduced the urine volume and sodium excretion without decreasing the glomerular filtration rate at 0.1 mg/kg (p.o.) in both IAP-treated and non-treated rats. Diuretic effects of KW-3902 (8-(noradamantan-3-yl)-1,3-dipropylxanthine) and 8-cyclopentyl-1,3-dipropylxanthine, adenosine A1-receptor antagonists, were not affected by pretreatment with IAP. These results suggest that endogenous adenosine may induce antidiuretic effects by accelerating the reabsorption of water and sodium at tubular sites via an IAP-insensitive mechanism, and that the diuretic effects of the adenosine A1-receptor antagonist may result from inhibiting this action of endogenous adenosine.
在百日咳毒素(IAP)处理和未处理的大鼠中测定了腺苷A1受体激动剂和拮抗剂的作用。腺苷A1激动剂(-)-N6-(2-苯异丙基)腺苷在IAP处理和未处理的大鼠中,以0.1mg/kg(口服)剂量给药时,可减少尿量和钠排泄,而不降低肾小球滤过率。腺苷A1受体拮抗剂KW-3902(8-(去甲金刚烷-3-基)-1,3-二丙基黄嘌呤)和8-环戊基-1,3-二丙基黄嘌呤的利尿作用不受IAP预处理的影响。这些结果表明,内源性腺苷可能通过IAP不敏感机制加速肾小管部位水和钠的重吸收来诱导抗利尿作用,并且腺苷A1受体拮抗剂的利尿作用可能是由于抑制了内源性腺苷的这一作用。