Background: Experimental evidence suggests that in conditions associated with an activated renin-angiotensin system, unopposed activity of angiotensin II underlies the marked renal vasoconstrictor response to nitric oxide synthase inhibition. In the present study, we investigated whether this holds true in hypertensive subjects pretreated with hydrochlorothiazide (HCT).
Methods: Systemic N(G)-nitro-L-arginine methyl ester (L-NAME) infusions (12.5 microg/kg per min for 40 min) were given to eight hypertensive subjects (age 53 +/- 6 years) during placebo, and during pretreatment with HCT (25 mg once daily) or HCT and losartan (LOS) (50 mg twice daily), both for 9 days. The glomerular filtration rate (GFR) and renal plasma flow were estimated from the clearances of radiolabeled thalamate and hippuran. Renal blood flow (RBF) was calculated as renal plasma flow/1 - hematocrit and the renal vascular resistance (RVR) as mean arterial pressure (MAP) divided by RBF.
Results: Compared with placebo, plasma renin increased (P < 0.001) from 15 +/- 4 mU/l during placebo to 26 +/- 7 mU/l during HCT and to 133 +/- 51 mU/l during HCT + LOS. MAP (110 +/- 3 mmHg) decreased to 102 +/- 4 mmHg during HCT and to 98 +/- 5 mmHg during HCT + LOS. RBF (579 +/- 36 ml/min), GFR (97 +/- 6 ml/min) and filtration fraction (29 +/- 2%) did not change, whereas RVR (200 +/- 15 RU) decreased to 183 +/- 13 RU during HCT and to 165 +/- 14 RU during HCT + LOS (P < 0.05). In response to L-NAME, MAP and RVR increased maximally by 10 +/- 3 and 67 +/- 9%, whereas RBF and GFR decreased maximally by 42 +/- 6 and 18 +/- 4%. Compared with these responses, the responses of MAP, RBF and RVR were not affected by pretreatment of HCT or HCT + LOS, but the L-NAME-induced decrease in GFR (26 +/- 5% during HCT and 29 +/- 5% during HCT and LOS) was enhanced (P < 0.01).
Conclusions: In hypertensive subjects with an activated renin-angiotensin system, unopposed activity of angiotensin II is not involved in L-NAME-induced pressor and renal vasoconstrictor response, whereas the L-NAME-induced decrease in GFR is enhanced, indicating greater dependency of GFR on nitric oxide-mediated vasodilator tone during sodium depletion.
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