Activation of NTS A 1 Adenosine Receptors Differentially Resets Baroreflex Control of Adrenal (ASNA) and Renal (RSNA) Sympathetic Nerve Activity

Previously we showed that pressor and differential sympathoexcitatory responses (ASNA>RSNA) to stimulation of NTS A 1 adenosine receptors were attenuated/abolished by baroreceptor denervation or blockade of glutamatergic transmission in the NTS, suggesting A 1 receptor‐elicited inhibition of glutamatergic transmission in baroreflex pathways ( Am J Physiol 283 : –99, 2002). Therefore we tested the hypothesis that stimulation of NTS A 1 adenosine receptors differentially inhibits/resets ASNA vs. RSNA baroreflex responses. In urethane/chloralose anesthetized male Sprague Dawley rats (n=6) we compared baroreflex‐response curves (MAP altered with iv. nitroprusside and phenylephrine) evoked before and after bilateral microinjections into the NTS of A 1 adenosine receptor agonist (CPA, 330 pmol/50 nL). Stimulation of NTS A 1 receptors evoked typical increases in MAP (25.8±4.0 mmHg), ASNA (98.5±18.6%) and RSNA (5.0±7.1%) and shifted baroreflex curves to higher MAP (by 53.7±4.0 and 42.2±5.0 mmHg for ASNA and RSNA, respectively) without altering the range of the responses. These shifts were not a result of simple baroreceptor resetting because the curves shifts were ~2 times greater than the increase in MAP evoked by stimulation of NTS A 1 adenosine receptors (P<0.05). Maximal gain tended to decrease for RSNA (5.3±1.6 vs. 2.7±0.3, P=0.120) and increase for ASNA (3.1±0.9 vs. 6.6±1.5, P=0.047). We conclude that activation of NTS A 1 adenosine receptors differentially inhibits baroreflex pathways controlling regional sympathetic outputs. NIH HL‐67814