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1 Department of Internal Medicine, Oregon Health & Science University, Portland, OR, USA; Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR, USA
2 Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: brooksv{at}ohsu.edu.
Nitric oxide (NO) appears to inhibit sympathetic tone in anesthetized rats. However, whether NO tonically inhibits sympathetic outflow, or whether endogenous Ang II promotes NO-mediated sympathoinhibition, in conscious rats is unknown. To address these questions, we determined the effects of nitric oxide synthase (NOS) inhibition on renal sympathetic nerve activity (RSNA) and heart rate (HR) in conscious, unrestrained rats on normal (NS), high (HS) and low sodium (LS) diets, in the presence and absence of an angiotensin II receptor antagonist (AIIRA). When arterial pressure was kept at baseline with intravenous hydralazine, NOS inhibition with L-NAME (10 mg Kg-1 i.v.) resulted in a profound decline in RSNA, to 42±11% of control (p<0.01), in NS animals. This effect was not sustained, and RSNA returned to control levels by 30 min post-infusion. L-NAME also caused bradycardia, from 432±23 b.p.m. to 372±11 b.p.m. post-infusion (p<0.01), an effect which, in contrast, was sustained 60 min post-drug. The effects of NOS inhibition on RSNA and HR did not differ between NS, HS and LS rats. However, when these animals were pre-treated with AIIRA, the initial decrease in RSNA following L-NAME was absent in the LS rats, while the response in the HS group was unchanged by AIIRA. These findings indicate that, in contrast to our hypotheses, NOS activity provides a stimulatory input to RSNA in conscious rats, and that in LS animals, but not HS animals, this sympathoexcitatory effect of NO is dependent on the action of endogenous Ang II.
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