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1 Max Delbrück Center for Molecular Medicine, 13122 Berlin-Buch, Germany; and 2 Oregon Health Sciences University, Portland, Oregon 97201
To determine whether increased sympathetic activity contributes
to the hypertension induced by chronic exposure to moderate nitric
oxide synthase (NOS) inhibition, various indexes of autonomic function
were measured in rats given the NOS inhibitor
NG-nitro-L-arginine methyl ester
(L-NAME, 10 mg/100 ml, 
16
mg · kg
1 · day1)
in the drinking water. One week of treatment raised blood pressure (139 ± 3 vs. 106 ± 1 mmHg; P < 0.01)
and lowered heart rate (319 ± 4 vs. 379 ± 6 beats/min,
P < 0.01).
L-NAME had no effect on cardiac
sympathetic tone, but elevated cardiac parasympathetic tone (
73 ± 4 vs. 56 ± 7 beats/min; P < 0.05). Depressor responses to ganglionic blockade were greater in
L-NAME-treated rats (50 ± 5 vs. 34 ± 5 mmHg; P < 0.05), whereas resting plasma, renal, and adrenal catecholamine values
did not differ between groups. Treated rats also showed evidence of
reduced baroreflex sympathetic stimulation of heart rate during
hypotension and reduced parasympathetic activation during hypertension.
Together, these data provide only very limited, indirect evidence that
sympathetic stimulation contributes to the hypertension associated with
moderate NOS inhibition.
chronic NG-nitro-L-arginine methyl ester; baroreflex
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