Yukimura T, Miura K, Ito K, Yamamoto K
J Cardiovasc Pharmacol. 1986 May-Jun;8(3):649-55. doi: 10.1097/00005344-198605000-00031.
The effects of different doses of dilazep on renal hemodynamics, urine formation, and renin release were studied in anesthetized dogs. Intrarenal arterial infusion of dilazep (1 microgram/kg/min) increased renal blood flow, with no change in systemic arterial blood pressure and renal venous plasma renin activity. Renal vasodilation induced by dilazep was completely inhibited by intrarenal arterial infusion of 3-isobutyl-1-methyl-xanthine (IBMX; 11.1 micrograms/kg/min), a potent adenosine receptor antagonist, but not by indomethacin (13 mg/kg i.v.). These results suggest that dilazep has a vasodilatory action in the kidney--one that is independent of the renal renin-angiotensin system. The inhibitory action of IBMX on the dilazep-induced renal vasodilation indicates that the renal vascular effects of dilazep may be exerted by augmentation of endogenous adenosine and mediated through adenosine receptors.
在麻醉犬中研究了不同剂量的双嘧达莫对肾血流动力学、尿液生成和肾素释放的影响。肾内动脉输注双嘧达莫（1微克/千克/分钟）可增加肾血流量，而全身动脉血压和肾静脉血浆肾素活性无变化。3-异丁基-1-甲基黄嘌呤（IBMX；11.1微克/千克/分钟，一种有效的腺苷受体拮抗剂）肾内动脉输注可完全抑制双嘧达莫诱导的肾血管舒张，但吲哚美辛（13毫克/千克静脉注射）则不能。这些结果表明双嘧达莫在肾脏具有血管舒张作用——一种独立于肾素-血管紧张素系统的作用。IBMX对双嘧达莫诱导的肾血管舒张的抑制作用表明，双嘧达莫的肾血管效应可能是通过内源性腺苷的增加而发挥作用，并通过腺苷受体介导。
