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1 Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA
2 Department of Exercise and Health Science, Yamaguchi University Faculty of Education, Yamaguchi, Japan
* To whom correspondence should be addressed. E-mail: tscislo{at}med.wayne.edu.
Our previous studies showed that preganglionic adrenal (pre-ASNA), renal (RSNA), lumbar, and postganglionic adrenal (post-ASNA) sympathetic nerve activities are inhibited following stimulation of arterial baroreceptors, NTS glutamatergic and P2x receptors and activated following stimulation of adenosine A1 receptors. However, stimulation of adenosine A2a receptors inhibited RSNA and post-ASNA, whereas activated pre-ASNA. Since the effects evoked by NTS A2a receptors may be mediated via activation of nitric oxide (NO) mechanisms in NTS neurons, we tested the hypothesis that NO synthase inhibitors would attenuate regional sympathetic responses to NTS A2a receptor stimulation whereas NO donors will evoke contrasting responses from pre-ASNA vs. RSNA and post-ASNA. Therefore, in chloralose/urethane anesthetized rats, we compared hemodynamic and regional sympathetic responses to microinjections of selective A2a receptor agonist (CGS21680, 20 pmol/50 nL) following pretreatment with NO synthase inhibitors (L-NAME 10 nmol/100 nL and TRIM 100 pmol/100 nL) vs. pretreatment with vehicle (100 nL). In addition, the responses to microinjections into the NTS of different NO donors (sodium nitroprusside, SNP, 40 and 400 pmol/50 nL; DETA NONOate, NOC18, 0.5 and 5 nmol/50 nL and PAPA NONOate, NOC15, 2 nmol/50 nL), the NO precursor, L-arginine (10-50 nmol/50 nL) and sodium glutamate (500 pmol/50 nL) were evaluated. SNP, NOC18 and NOC15 activated pre-ASNA and inhibited RSNA and post-ASNA whereas L-arginine and glutamate microinjected into the same site of the NTS inhibited all these sympathetic outputs. Decreases in heart rate and depressor or biphasic responses accompanied the neural responses. Pretreatment with NO synthase inhibitors reversed the normal depressor and sympathoinhibitory responses to stimulation of NTS A2a receptors into pressor and sympathoactivatory responses and attenuated the heart rate decreases; however it did not change the increases in pre-ASNA. We conclude that NTS NO mechanisms differentially affect regional sympathetic outputs and differentially contribute to the pattern of regional sympathetic responses evoked by stimulation of NTS A2a receptors.
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