L-Arginine improves endothelial function in renal artery of hypertensive Dahl rats

Objectives To clarify whether endothelium-derived contracting factor (EDCF) is developed in renal artery of hypertensive Dahl rats and whether prolong ed oral L-arginine treatments prevent development of EDCF and hypertension. Design The effect of prolonged salt treatment with or without L-arginine on the renal artery was examined. Methods and Results Dahl salt-sensitive and -resistant rats were fed a 0.4 or an 8% NaCl diet for 4 weeks. High sodium intake increased arterial press ure in Dahl salt-sensitive rats, The rings of renal arteries were suspended for isometric tension recording. Only in the hypertensive rats, more than 1 mu mol/l acetylcholine induced an endothelium-dependent contraction respo nse. The contraction was completely inhibited by indomethacin or ONO-3708 [ prostaglandin H-2 (PGH(2))/thromboxane A(2) (TXA(2)) receptor antagonist], and partially inhibited by OKY-046 (TXA(2) synthetase inhibitor). Acetylcho line-induced relaxation was significantly depressed in hypertensive rats, w hich was partially improved by SQ29548 (PGH(2)/TXA(2) receptor antagonist). Oral L-arginine, but not ONO-8809 (orally active PGH(2)/TXA(2) receptor an tagonist) treatment, inhibited the contraction and amended the relaxation, The endothelium-independent contraction to TXA(2) receptor agonist U46619 a nd relaxation to nitroprusside were not altered by L-arginine treatment. Th e L-Arginine treatment reduced blood pressure and sodium retention with inc reases in urinary NO2-/NO3- and cGMP excretion. Hydralazine treatment also inhibited development of EDCF. Conclusions The present results suggest that impaired endothelium-dependent relaxation to acetylcholine is caused in part by induction of EDCF synthes is/release in renal arteries of hypertensive Dahl rats. L-arginine can atte nuate sodium retention and development of hypertension, which lead to a dec rease in EDCF synthesis in renal arteries, J Hypertens 19:421-429 (C) 2001 Lippincott Williams & Wilkins.