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Severe hemorrhage attenuates cardiopulmonary chemoreflex (CCR) control of renal and adrenal sympathetic nerves via adenosine operating in the nucleus of the solitary tract (NTS)
Author(s) -
Minic Zeljka,
Li Cailian,
O'Leary Donal S,
Scislo Tadeusz J.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1118.13
Subject(s) - adenosine , adenosine receptor , agonist , medicine , endocrinology , adenosine a2a receptor , adenosine a1 receptor , purinergic signalling , blockade , receptor
During severe hemorrhage adrenal sympathoactivation is accompanied by paradoxical renal sympathoinhibition and bradycardia. Adenosine operating in the NTS via A 1 and A 2a receptors contributes to the paradoxical effects and it inhibits CCR mediated sympathoinhibition ( Am J Physiol 291: H2453‐H2461, 2006; 303: R539‐R550, 2012; FASEB J 25: 844.3, 2011). Therefore, we hypothesized that adenosine released into the NTS during severe hemorrhage will attenuate the CCR and that blockade of NTS adenosine receptors will reverse this attenuation. We compared renal and adrenal sympathetic responses evoked by right atrial injections of 5HT 3 receptor agonist, phenylbiguanide (PBG, 1–8 μg/kg), under control conditions, during hemorrhage and during hemorrhage after blockade of NTS adenosine receptors with bilateral microinjections of 8‐(p‐sulfophenyl) theophylline (1 nmol/100 nl) in urethane/chloralose anesthetized rats. Hemorrhage significantly attenuated the CCR responses and blockade of NTS adenosine receptors reversed this attenuation. We conclude that adenosine released into the NTS contributes to the paradoxical posthemorrhagic effects but it also serves as a negative feedback regulator of the CCR. HL‐67814