RENAL VERSUS FEMORAL HEMODYNAMIC-RESPONSE TO ENDOTHELIUM-DERIVED RELAXING FACTOR SYNTHESIS INHIBITION

Systemic inhibition of endothelium-derived relaxing factor (EDRF) synt hesis leads to acute hypertension and increased peripheral vascular re sistance. The changes in vascular resistance are not evenly distribute d to all vascular beds. In this study, we compared the renal and femor al hemodynamic responses to EDRF synthesis inhibition. Renal blood flo w (RBF) and femoral blood flow (FBF) were assessed in the presence and absence of DuP 753, an angiotensin II receptor antagonist. Inhibition of EDRF synthesis by a bolus dose of L(w)-nitroarginine methyl ester (L-NAME) increased blood pressure (BP) by 21 +/- 1 mm Hg (p < 0.001) a nd decreased RBF by 32 +/- 5% (from 5.9 +/- 0.5 to 3.9 +/- 0.3 ml/min/ g kidney weight; p < 0.005) while FBF remained unchanged (9.5 +/- 0.4 versus 9.4 +/- 0.4 ml/min). Renal vascular resistance (RVR) increased by 83 +/- 16% (p < 0.001), compared with only a 24 +/- 6% increase in femoral vascular resistance (FVR; p < 0.005). To eliminate the influen ce of systemic hypertension, we returned organ perfusion pressure to p re-L-NAME levels by partial aortic constriction. The kidney maintained RBF by decreasing RVR by 8 +/- 2% (p < 0.02), while FBF decreased by 15 +/- 5% (p < 0.01). When rats were pretreated with DuP 753, L-NAME s till increased BP by 22 +/- 2 mm Hg, but RVR increased by only 26 +/- 5% (from 13.2 +/- 1.6 to 16.8 +/- 2.7; p < 0.01) and RBF did not chang e. DuP 753 had no effect on the femoral vascular response to L-NAME. F BF did not change (9.3 +/- 0.2 versus 9.8 +/- 0.7), while FVR increase d by 23 +/- 3% (from 8.7 +/- 0.3 to 10.8 +/- 0.6; p < 0.001). These re sults suggest that EDRF is a more important regulator of RBF than of F BF. We conclude that the kidney has a disproportionate reliance on EDR F to maintain RBF compared to FBF.