Chronic nitric oxide inhibition with l-NAME: effects on autonomic control of the cardiovascular system

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Abstract
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 N G-nitro-l-arginine methyl ester (l-NAME, 10 mg/100 ml, ≅16 mg ⋅ kg−1 ⋅ day−1) 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 inl-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.