Romero J C, Strong C G
Mayo Clin Proc. 1977 Jul;52(7):462-4.
Blockade of prostaglandin synthesis with indomethacin (1) did not induce significant changes in blood pressure or in renal circulation in renovascular hypertensive rabbits with normal renal blood flow; (2) induced renal insufficiency and aggravated hypertension in hypertensive rabbits whose renal blood flow was below normal levels; (3) did not alter the reversal of renovascular hypertension produced by the release of the renal arterial constriction; and (4) induced a decrease in plasma renin activity by decreasing renin release. These findings indicate that the vasodilator and natriuretic actions of prostaglandins may play an important role in protecting the kidney against ischemia; the facilitating role of renal prostaglandins on renin release raises the possibility that a primary hypersecretion of renal prostaglandins is responsible for Bartter's syndrome, whereas a primary deficiency may be responsible for "low-renin hypertension."
（1）在肾血流正常的肾血管性高血压兔中，未引起血压或肾循环的显著变化；（2）在肾血流低于正常水平的高血压兔中，诱发了肾功能不全并加重了高血压；（3）未改变肾动脉缩窄解除后肾血管性高血压的逆转；（4）通过减少肾素释放而导致血浆肾素活性降低。这些发现表明，前列腺素的血管舒张和利钠作用可能在保护肾脏免受缺血方面起重要作用；肾脏前列腺素对肾素释放的促进作用增加了原发性肾脏前列腺素分泌过多导致巴特综合征的可能性，而原发性缺乏可能导致“低肾素性高血压”。
