[Caffeine inhibits chemoreceptor responses to hypoxia.]

[Caffeine inhibits chemoreceptor responses to hypoxia.] Research Abstract Details 

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[Caffeine inhibits chemoreceptor responses to hypoxia.] Abstract Text:

Sv Conde,A Obeso,Ec Monteiro,R Rigual,C Gonzalez,

Patients with obstructive sleep apnoea (OSA) are high con- sumers of caffeine. Different molecular mechanisms have been attributed to caffeine, but probably the most impor- tant effect achieved with low concentrations (1-100 microM) is the antagonism of adenosine receptors. For example, the stimulatory effect of caffeine in the treatment of newborn apnoea is due to the inhibition of A(1) (and probably A(2A)) adenosine receptors in central respiratory neurons (Mazza- relli et al., 1986 J. Appl. Physiol. 60, 52-56; Herlenius and La- gercrantz, 1999, J Physiol. 518, 159-172). In premature babi- es the hyperventilatory response to hypoxia mediated by peripheral chemoreceptors is reduced and contrasts with the opposite effect observed in adults suffering from OSA where an augmented carotid body sensory response to hypoxia has been shown (Pen & Prabhakar, 2004, J. Appl. Physiol., 96, 1236-1242; Rey et al., 2004, J.Physiol., 560, 577-586). The present work was based in the hypothesis that caffeine could modify chemoreflex activity in OSA and therefore contribute to systemic consequences of intermittent hypo- xia. We started exploring this hypothesis investigating the effects of caffeine in carotid body chemoreceptor activity in a rat model. Experiments were performed in vitro and carotid body res- ponses to hypoxia were assessed quantifying the release of ca- techolamines and carotid sinus nerve (CSN) activity. Immuno- cytochemical techniques were also used to confirm the presence of adenosine receptors that have been characterised pharma- cologically as being the targets for caffeine at the carotid body. Dose-response curves for caffeine (1nM-10mM) in the absen- ce and in the presence of selective adenosine antagonists were obtained in the two experimental preparations. Caffeine inhibited (IC(50), 210 microM) both the basal release of catecholamines from chemoreceptor cells and the release evoked by a low intensity of hypoxia for in vitro studies (PO(2) congruent with 66 mmHg). Opposite to caffeine, NECA (adenosine A(2) agonist) augmented basal and low intensity hypoxia induced release of catecholamines. CGS21680, HE-NECA (A(2A) re- ceptor agonists) and SCH58621 (A(2A) receptor antagonist) did not affect neither the release nor the caffeine effects. DPCPX (A(1)/A(2B) antagonist) and MRS1754 (A(2B) antagonist) mimicking caffeine indicated that caffeine effects were me- diated by A(2B) receptors. Immunocytochemical A(2B) recep- tors were identified in tyrosine hydroxylase positive chemo- receptor cells. Caffeine reduced (52%) the chemosensory discharges elicited by hypoxia in the carotid sinus nerve. Inhi- bition had two components with pharmacological analysis indicating that A(2A) and A(2A) receptors mediate, respectively, the low (17x10(-9) M) and high (160x10(-6) M) IC(50) effects. It is conclude that caffeine has an inhibitory effect on caro- tid body chemoreceptor responses to hypoxia acting throu- gh the antagonism of adenosine receptors. This effect su- ggests that caffeine could modify the consequences of chemoreceptor activation by intermittent hypoxia (e.g. hyper- tension) and stimulates further studies to investigate its effects in patients with OSA. Key-words: Caffeine, Carotid body, Hypoxia, Obstructive sleep apnea.

[Caffeine inhibits chemoreceptor responses to hypoxia.] Publishing Authors By Initials

S Conde,A Obeso,E Monteiro,R Rigual,C Gonzalez,

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[Caffeine inhibits chemoreceptor responses to hypoxia.] Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Revista portuguesa de pneumologia

VOLUME: 12

Page Numbers: 56-7

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ISSN: 0873-2159

DAY: 8

MONTH: Dec

YEAR: 2006

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LANGUAGE: por

NlmUniqueID: 9813736

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AFFILIATION: Department of Biochemistry, Molecular Biology and Physio- logy, Faculty of Medicine, University of Valladolid, CSIC, Valla- dolid, Spain; Department of Pharmacology, Faculty of Medi- cal Sciences, New University of Lisbon, Lisbon, Portuga.

Country: Portugal

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MEDLINETA: Rev Port Pneumol

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