Differential interactions between NTS adenosine A 2a and GABA A receptors in control of renal (RSNA) and adrenal (ASNA) sympathetic nerve activity

Activation of NTS A 2a adenosine receptors decreases RSNA, mean arterial pressure (MAP) and heart rate (HR) whereas it increases ASNA ( Clin Exp Physiol Pharmacol 28: 120–124, 2001). Only the increases in ASNA are attenuated by ionotropic glutamatergic blockade or sinoaortic denervation + vagotomy suggesting that some of adrenal sympathoexcitation may be mediated via GABA‐ergic inhibition of sympathoinhibitory reflexes. Therefore in the present study we tested hypothesis, that blockade of NTS GABA A receptors will attenuate the increases in ASNA. In urethane/chloralose anesthetized rats (n=12) we compared the hemodynamic and neural responses to stimulation of NTS A 2a adenosine receptors (microinjections of CGS21680, 20 pmol/50 nl) evoked after pretreatment with vehicle (100nl) or GABA A antagonist, bicuculline (10pmol/100nl). Bicuculline decreased typical adrenal sympathoexcitation (55±5 vs. 41±3 Δ%), as expected. Surprisingly, the typical decreases in RSNA, MAP and HR were reversed in this setting (−48±5 vs. 52±7 Δ%, −29±4 vs. 37±9 Δ% and −40±7 vs. 18±3bpm, respectively). This suggests that the increases in ASNA may partially depend on GABA‐ergic inhibition of reflex sympathoinhibitory pathways. In contrast, the decreases in RSNA, MAP and HR may be mediated via GABA‐ergic inhibition of tonic descending, nonglutamatergic projections to the NTS which tonically activate these variables. NIH HL‐67814