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Activation of NTS A_2a adenosine receptors differentially resets baroreflex control of renal vs. adrenal sympathetic nerve activity

¹Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan; and ²Osaka International University, Osaka, Japan

Submitted 18 August 2008 ; accepted in final form 28 January 2009

The role of nucleus of solitary tract (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 (intravenous 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.

A_2a adenosine receptor agonist; A_2a adenosine receptor antagonist; baroreflex function; renal nerve; adrenal nerve

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