Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent

Abstract

Recent studies have indicated that chronic administration of Nω-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, produces marked hypertension. Although the mechanism of this form of hypertension is not well understood, several studies have demonstrated that sympathetic nerve activity is at least acutely elevated after L-NAME administration. To evaluate the potential role of the renal sympathetic nerves in L-NAMEinduced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n=8 each): (1) sham-operated vehicle-treated, (2) shamoperated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. After renal denervation or sham surgery, L-NAME was added to the drinking water (70 mg/100 mL) for 4 weeks, and arterial pressure was measured weekly by the tail-cuff method. L-NAME treatment caused a progressive increase in arterial pressure in shamoperated rats, rising to 154±6 mm Hg by week 4 of treatment compared with 115±2 mm Hg in the vehicle-treated shamoperated group (P