Activation of NTS A1 adenosine receptors impairs cardiopulmonary chemoreflex responses of adrenal (ASNA), lumbar (LSNA) and renal (RSNA) sympathetic nerve activity

Abstract

Activation of NTS A1 adenosine receptors evokes differential sympathoactivation (ASNA>RSNA≥LSNA). These responses were attenuated/abolished by sinoaortic denervation plus vagotomy or blockade of glutamatergic transmission in the NTS suggesting that these receptors may inhibit baroreflex transmission in the NTS (Am J Physiol 283: H1588‐99, 2002; 294: H172‐82, 2008). However, potential inhibition of cardiopulmonary chemoreceptors may also contribute to the A1 adenosine‐receptor‐mediated differential regional sympathoactivation. Therefore, in the present study we compared regional sympathoinhibition evoked by right atrial injections of 5HT3 receptor agonist (phenylbiguanide (PBG) 1‐8 μg/kg) before and after stimulation of NTS A1 adenosine receptors (microinjections of CPA, 330 pmol/50 nl) in urethane/chloralose anesthetized rats (n=7). Activation of cardiopulmonary chemoreceptors evoked differential, dose dependent sympathoinhibition (RSNA>ASNA>LSNA). The responses to all doses of PBG (Δ%) were greatly attenuated following stimulation of NTS A1 adenosine receptors (‐95.6±1.2 vs. ‐40.4±8.5, ‐75.4±5.8 vs. ‐27.5±6.8, ‐60.9±3.3 vs. ‐29.1±7.3, for RSNA, ASNA and LSNA respectively at the maximal dose of PBG). We conclude that activation of A1 adenosine receptors in the NTS differentially inhibits the cardiopulmonary chemoreflex responses of regional sympathetic outputs. NIH HL‐67814