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  • Title: Effect of inhibition of nitric oxide synthase on blood pressure and renal sodium handling in renal denervated rats.
    Author: Xavier F, Magalhães AM, Gontijo JA.
    Journal: Braz J Med Biol Res; 2000 Mar; 33(3):347-54. PubMed ID: 10719388.
    Abstract:
    The role of sympathetic nerve activity in the changes in arterial blood pressure and renal function caused by the chronic administration of N G-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, was examined in sham and bilaterally renal denervated rats. Several studies have demonstrated that sympathetic nerve activity is elevated acutely after L-NAME administration. To evaluate the role of renal nerve activity in L-NAME-induced hypertension, we compared the blood pressure response in four groups (N = 10 each) of male Wistar-Hannover rats weighing 200 to 250 g: 1) sham-operated vehicle-treated, 2) sham-operated L-NAME-treated, 3) denervated vehicle-treated, and 4) denervated L-NAME-treated rats. After renal denervation or sham surgery, one control week was followed by three weeks of oral administration of L-NAME by gavage. Arterial pressure was measured weekly in conscious rats by a tail-cuff method and renal function tests were performed in individual metabolic cages 0, 7, 14 and 21 days after the beginning of L-NAME administration. L-NAME (60 mg kg-1 day-1) progressively increased arterial pressure from 108 +/- 6.0 to 149 +/- 12 mmHg (P<0.05) in the sham-operated group by the third week of treatment which was accompanied by a fall in creatinine clearance from 336 +/- 18 to 222 +/- 59 microl min-1 100 g body weight-1 (P<0. 05) and a rise in fractional urinary sodium excretion from 0.2 +/- 0. 04 to 1.62 +/- 0.35% (P<0.05) and in sodium post-proximal fractional excretion from 0.54 +/- 0.09 to 4.7 +/- 0.86% (P<0.05). The development of hypertension was significantly delayed and attenuated in denervated L-NAME-treated rats. This was accompanied by a striking additional increase in fractional renal sodium and potassium excretion from 0.2 +/- 0.04 to 4.5 +/- 1.6% and from 0.1 +/- 0.015 to 1.21 +/- 0.37%, respectively, and an enhanced post-proximal sodium excretion compared to the sham-operated group. These differences occurred despite an unchanged creatinine clearance and Na+ filtered load. These results suggest that bilateral renal denervation delayed and attenuated the L-NAME-induced hypertension by promoting an additional decrease in tubule sodium reabsorption in the post-proximal segments of nephrons. Much of the hypertension caused by chronic NO synthesis inhibition is thus dependent on renal nerve activity.
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