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Central Adenosine Receptors Differentially Contribute To The Nicotine‐Induced Attenuation Of Reflex Tachycardic Responses To Baroreceptor Unloading
Author(s) -
ElMas Mahmoud M,
Elgowilly Sahar M,
Fouda Mohamed A,
Saad Evan I
Publication year - 2011
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.25.1_supplement.1084.3
Subject(s) - baroreceptor , nicotine , reflex , adenosine , adenosine receptor , medicine , receptor , neuroscience , anesthesia , blood pressure , biology , heart rate , agonist
Nicotine impairs reflex cardiac sympathoexcitatory responses to baroreceptor unloading. The role of central adenosine receptors in the nicotine‐baroreflex interaction was investigated. Baroreflex curves relating reflex heart rate (HR) responses to decreases in blood pressure (BP) evoked by i.v. doses (1–16 μg/kg) of sodium nitroprusside (SNP) was constructed in conscious male rats. Slopes of the curves were taken as a measure of baroreflex sensitivity (BRS SNP ). Whether administered i.v. (25 or 100 μg/kg) or intracis‐ternally (2 or 5 μg/rat), nicotine caused dose‐dependent downward shifts in SNP curves and reductions in BRS SNP . BRS SNP was also reduced in rats treated intracisternally with 8‐phenyltheophylline (8‐PT, nonselective adenosine receptor antagonist), 8‐(3‐Chlorostyryl) caffeine (CSC, A 2A antagonist), or VUF5574 (A 3 antagonist) in contrast to no effect for DPCPX (A 1 antagonist), alloxazine (A 2B antagonist), or dipyridamole (adenosine uptake inhibitor). Pretreatment with 8‐PT or CSC abrogated the BRS SNP depressant effect of nicotine whereas other adenosine receptor antagonists were without effect. It is concluded that central pathways of A 2A or A 3 receptors tonically facilitate reflex cardiac sympathoexcitation. Further, disruption of central A 2A receptor signaling mediates the nicotine‐baroreflex interaction. Supported by Faculty of Pharmacy, Alexandria University, Egypt.