The role of NTS A_2a adenosine receptors in baroreflex mechanisms is controversial. Stimulation of these receptors releases glutamate within the NTS and elicits baroreflex like decreases in mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA), whereas inhibition of these receptors attenuates HR baroreflex responses. In contrast, stimulation of NTS A_2a adenosine receptors increases preganglionic adrenal sympathetic nerve activity (pre-ASNA) and the depressor and sympathoinhibitory responses are not markedly affected by sinoaortic denervation and blockade of NTS glutamatergic transmission. To elucidate the role of NTS A_2a adenosine receptors in baroreflex function we compared full baroreflex stimulus-response curves for HR, RSNA and pre-ASNA (i.v. nitroprusside/phenylephrine) before and after bilateral NTS microinjections of selective adenosine A_2a receptor agonist (CGS-21680; 2.0, 20 pmol/50 nl), selective A_2a receptor antagonist (ZM-241385; 40 pmol/100 nl), and nonselective A₁ + A_2a receptor antagonist (8-SPT; 1 nmol/100 nl) in urethane/-chloralose anesthetized rats. Activation of A_2a receptors decreased the range, upper plateau and gain of baroreflex-response curves for RSNA whereas these parameters all increased for pre-ASNA, consistent with direct effects of the agonist on regional sympathetic activity. However, no resetting of baroreflex-response curves along the MAP axis occurred despite the marked decreases in baseline MAP. The antagonists had no marked effects on baseline variables or baroreflex-response functions. We conclude that the activation of NTS A_2a adenosine receptors differentially alters baroreflex control of HR, RSNA and pre-ASNA mostly via non-baroreflex mechanism(s) and these receptors have virtually no tonic action on baroreflex control of these sympathetic outputs.