Renal denervation significantly delayed and attenuated the development of L-NAME-induced hypertension in rats, which rose to 154 mm Hg in sham-operated rats vs 115 mm Hg in controls (P<.005).
Absolute Event Rate: 154% vs 115%
p-value: p=<.005
Recent studies have indicated that chronic administration of N omega-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-NAME-induced 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) sham-operated 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 sham-operated rats, rising to 154 +/- 6 mm Hg by week 4 of treatment compared with 115 +/- 2 mm Hg in the vehicle-treated sham-operated group (P < .005). In contrast, the development of hypertension was significantly delayed and attenuated in renal-denervated rats treated with L-NAME. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves.
Matsuoka et al. (Wed,) conducted a other in Hypertension (n=32). Renal denervation + L-NAME vs. Sham surgery + L-NAME, and vehicle controls was evaluated on Arterial pressure at 4 weeks (p=<.005). Renal denervation significantly delayed and attenuated the development of L-NAME-induced hypertension in rats, which rose to 154 mm Hg in sham-operated rats vs 115 mm Hg in controls (P<.005).