Hypertension, Vol 23, 971-975, Copyright © 1994 by American Heart Association
H Matsuoka, H Nishida, G Nomura, BN Van Vliet and H Toshima
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.
ARTICLES
Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent
Third Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
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