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1Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan; and 2Osaka International University, Osaka, Japan
Submitted 21 September 2007 ; accepted in final form 31 October 2007
Previously we showed that pressor and differential regional sympathoexcitatory responses (adrenal > renal 
lumbar) evoked by stimulation of A1 adenosine receptors located in the nucleus of the solitary tract (NTS) were attenuated/abolished by baroreceptor denervation or blockade of glutamatergic transmission in the NTS, suggesting A1 receptor-elicited inhibition of glutamatergic transmission in baroreflex pathways. Therefore we tested the hypothesis that stimulation of NTS A1 adenosine receptors differentially inhibits/resets baroreflex responses of preganglionic adrenal (pre-ASNA), renal (RSNA), and lumbar (LSNA) sympathetic nerve activity. In urethane-chloralose-anesthetized male Sprague-Dawley rats (n = 65) we compared baroreflex-response curves (iv nitroprusside and phenylephrine) evoked before and after bilateral microinjections into the NTS of A1 adenosine receptor agonist (N6-cyclopentyladenosine, CPA; 0.033–330 pmol/50 nl). CPA evoked typical dose-dependent pressor and differential sympathoexcitatory responses and similarly shifted baroreflex curves for pre-ASNA, RSNA, and LSNA toward higher mean arterial pressure (MAP) in a dose-dependent manner; the maximal shifts were 52.6 ± 2.8, 48.0 ± 3.6, and 56.8 ± 6.7 mmHg for pre-ASNA, RSNA, and LSNA, respectively. These shifts were not a result of simple baroreceptor resetting because they were two to three times greater than respective increases in baseline MAP evoked by CPA. Baroreflex curves for pre-ASNA were additionally shifted upward: the maximal increases of upper and lower plateaus were 41.8 ± 16.4% and 45.3 ± 8.7%, respectively. Maximal gain (%/mmHg) measured before vs. after CPA increased for pre-ASNA (3.0 ± 0.6 vs. 4.9 ± 1.3), decreased for RSNA (4.1 ± 0.6 vs. 2.3 ± 0.3), and remained unaltered for LSNA (2.1 ± 0.2 vs. 2.0 ± 0.1). Vehicle control did not alter the baroreflex curves. We conclude that the activation of NTS A1 adenosine receptors differentially inhibits/resets baroreflex control of regional sympathetic outputs.
nucleus of the solitary tract; purinergic receptors; adrenal nerve; renal nerve; lumbar nerve; pressor reflex
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