Nijkamp F P, de Jong W
Arch Int Pharmacodyn Ther. 1984 Apr;268(2):259-70.
Application of a solid renal artery clip (0.25 mm i.d.) in rats with an undisturbed contralateral kidney (two-kidney one clip renal hypertension; 2KH ) causes a small increase in blood pressure within the first 3 hr. After pretreatment of the animals with aspirin the blood pressure response was enhanced. In contrast, in unilaterally nephrectomized rats after clipping(one-kidney one clip renal hypertension; 1KH ), the increase in blood pressure of the control and aspirin pretreated group was similar and at the level of the aspirin pretreated group of the 2KH -rats. One day after clipping in the 2KH -rats there was still a marked enhancement of the blood pressure increase induced by the prostaglandin-synthesis inhibitor. Plasma renin activity of the aspirin and control group 1 hr after clipping was significantly increased as compared to the sham operated animals in as well the 2KH - and 1KH -rats. The converting enzyme inhibitor captopril attenuates the acute increase in blood pressure in both control and aspirin treated 2KH - and 1KH -rats pointing to a major role for angiotensin II. It is suggested that the potentiation of blood pressure after prostaglandin synthesis inhibition is due to a diminished release of prostaglandins by the contralateral kidney. The data indicate that in intact rats prostaglandins may act as breaking mechanism against hypertensive influences such as a sudden increase in blood pressure by angiotensin II.
在对侧肾脏未受干扰的大鼠（两肾一夹肾性高血压；2KH）中应用实心肾动脉夹（内径0.25毫米），会在最初3小时内使血压略有升高。在用阿司匹林预处理动物后，血压反应增强。相比之下，在单侧肾切除术后夹闭的大鼠（一肾一夹肾性高血压；1KH）中，对照组和阿司匹林预处理组的血压升高情况相似，且处于2KH大鼠阿司匹林预处理组的水平。在2KH大鼠夹闭后一天，前列腺素合成抑制剂诱导的血压升高仍有显著增强。与假手术动物相比，夹闭后1小时，2KH和1KH大鼠的阿司匹林组和对照组的血浆肾素活性均显著升高。转化酶抑制剂卡托普利可减弱对照组和阿司匹林处理的2KH和1KH大鼠的血压急性升高，这表明血管紧张素II起主要作用。有人认为，前列腺素合成抑制后血压的增强是由于对侧肾脏前列腺素释放减少。数据表明，在完整大鼠中，前列腺素可能作为一种对抗高血压影响的制动机制，如血管紧张素II导致的血压突然升高。
