Renal vascular interaction of angiotensin II and prostaglandins in renovascular hypertension

The vascular responses to angiotensin II (Ang II) in the renal circulation are increased in kidneys from rats with aortic coarctation compared with sh am-operated rats. We have suggested that these differences are related to c hanges in mediators of the Ang II effect. The aim of this study was to inve stigate the role of arachidonic acid (AA) metabolites on the Ang II effect in the renal circulation of normotensive and hypertensive rats. We evaluate d vascular renal reactivity in the rat isolated perfused kidney. Bolus inje ction of Ang II (9, 18, 36, 72 ng) increased perfusion pressure in a dose-d ependent manner by 16.5 +/- 4, 23.5 +/- 4, 35.5 +/- 7, and 42.5 +/- 7 mm Hg in sham-operated rats and 50 +/- 6, 72 +/- 10, 92 +/- 6, and 120 +/- 6 mm Hg in rats with aortic coarctation. Ang II-induced vasoconstriction was pre vented in hypertensive rats and potentiated in normotensive rats by the pre sence of indomethacin(1 mu g/ml) in the perfusion solution. Furthermore, th e use of the endoperoxide/thromboxane blocker (SQ29548, 1 mu M) did not alt er the effect of Ang Il on the normotensive rats but prevented its effect i n hypertensive rats. Moreover, the prostaglandin/ thromboxane (PGH(2)/TxA(2 )) receptor agonist U46619 increased perfusion pressure to similar values i n both kidneys from sham-operated or aortic coarctation rats. Ang II stimul ated AA and prostaglandin release from isolated perfused kidneys. However, autacoid release was higher in kidneys from rats with aortic coarctation. I n conclusion, we suggest that during the development of hypertension, the A A metabolism of vasoconstrictor prostaglandins is increased, and it mediate s the vasoconstrictive effects of Ang II.