Stimulation of NTS Ai adenosine receptors differentially resets baroreflex control of regional sympathetic outputs

摘要

First published November 2, 2007; doi: 10.1152/ajpheart.01099.2007.-Previously we showed that pressor and differential regional sympathoexcitatory responses (adrenal > renal = lumbar) evoked by stimulation of Ai 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 Ai receptor-elicited inhibition of glutamatergic transmission in baroreflex pathways. Therefore we tested the hypothesis that stimulation of NTS Ai 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 Ai 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 Ai adenosine receptors differentially inhibits/resets baroreflex control of regional sympathetic outputs.