Respiratory and body temperature modulation by adenosine A1 receptors in the anteroventral preoptic region during normoxia and hypoxia

Barros, Renata C.H.; Branco, Luiz G.S.; Cárnio, Evelin C.

doi:10.1016/j.resp.2005.09.013

Cited by 37 publications

(24 citation statements)

References 41 publications

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“…However, systemic administration of selective A 2A R agonists can increase HR, probably due to reflex activation secondary to reduced blood pressure (6,31,32,34,35). In addition, there is evidence that there are ARs in the brain stem regulating cardiovascular control centers (2)(3)(4).…”

Section: Discussionmentioning

confidence: 99%

Physiological roles of A₁ and A_2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine

Yang

Chen²,

Fredholm³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Yang JN, Chen JF, Fredholm BB. Physiological roles of A1 and A2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine. Am J Physiol Heart Circ Physiol 296: H1141-H1149, 2009. First published February 13, 2009 doi:10.1152/ajpheart.00754.2008.-Heart rate (HR), body temperature (Temp), locomotor activity (LA), and oxygen consumption (O2C) were studied in awake mice lacking one or both of the adenosine A 1 or A2A receptors (A1R or A2AR, respectively) using telemetry and respirometry, before and after caffeine administration. All parameters were lower during day than night and higher in females than males. When compared with wild-type (WT) littermates, HR was higher in male A 1R knockout (A1RKO) mice but lower in A2ARKO mice and intermediate in A1-A2AR double KO mice. A single dose of an unselective ␤-blocker (timolol; 1 mg/kg) abolished the HR differences between these genotypes. Deletion of A 1Rs had little effect on Temp, whereas deletion of A 2ARs increased it in females and decreased it in males. A 1-A2ARKO mice had lower Temp than WT mice. LA was unaltered in A 1RKO mice and lower in A 2ARKO and A1-A2ARKO mice than in WT mice. Caffeine injection increased LA but only in mice expressing A 2AR. Caffeine ingestion also increased LA in an A 2AR-dependent manner in male mice. Caffeine ingestion significantly increased O 2C in WT mice, but less in the different KO mice. Injection of 30 mg/kg caffeine decreased Temp, especially in KO mice, and hence in a manner unrelated to A 1R or A 2AR blockade. Selective A2B antagonism had little or no effect. Thus A 1R and A2AR influence HR, Temp, LA, and O2C in mice in a sex-dependent manner, indicating effects of endogenous adenosine. The A2AR plays an important role in the modulation of O2C and LA by acute and chronic caffeine administration. There is also evidence for effects of higher doses of caffeine being independent of both A 1R and A2AR. diurnal rhythm; metabolic rate; locomotor activity; adenosine; telemetry CAFFEINE (1,3,7-trimethylxanthine), the most widely consumed stimulant in the world, acts as a competitive antagonist of adenosine receptors (ARs) (18). It is much more potent on three of the known receptors, A 1 , A 2A , and A 2B (A 1 R, A 2A R, and A 2B R, respectively) than on the fourth, the A 3 R (17). Since a competitive antagonist will have effects only when and where receptors are activated by an agonist, it is relevant that endogenous agonist adenosine is more potent on A 1 R and A 2A R than on A 2B R. The potency of adenosine as an agonist in addition depends on the density of the receptors (16). The levels of adenosine are low under physiological condition but are sufficient to partially activate A 1 R, A 2A R, and A 3 Rs where the receptors are abundantly expressed. For these reasons caffeine is generally believed to act on A 1 R and A 2A R to exert most of its effects, at least when given in lower doses (18). However, a recent study showed that A 2B R knockout (A 2B RKO) mice have e...

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Section: Discussionmentioning

confidence: 99%

Physiological roles of A₁ and A_2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine

Yang

Chen²,

Fredholm³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Novoa et al, 1991;Kilgore et al, 2007) and other vertebrate classes suggests that the mechanisms responsible for T b depression are widespread; however, responses of the thermoregulatory control system to hypoxia are still poorly understood (Bicego et al, 2007). Previous studies in mammals indicate that hypothalamic O 2 sensors may initiate T b depression during hypoxia, and can operate in absence of peripheral chemoreceptor inputs (Iriki and Kozawa, 1976;Fewell et al, 1997;Barros et al, 2006;Gargaglioni et al, 2006). Our findings suggest that this could also be the case in birds: vagotomy, which in birds eliminates afferent input from all arterial and pulmonary chemoreceptors, did not eliminate T b depression during hypoxia in ducks (Fig.·8A).…”

Section: Hypoxic Responses Of Waterfowlmentioning

confidence: 99%

Body temperature depression and peripheral heat loss accompany the metabolic and ventilatory responses to hypoxia in low and high altitude birds

Scott

Cadena

Tattersall

et al. 2008

Journal of Experimental Biology

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SUMMARYThe objectives of this study were to compare the thermoregulatory, metabolic and ventilatory responses to hypoxia of the high altitude bar-headed goose with low altitude waterfowl. All birds were found to reduce body temperature (T b ) during hypoxia, by up to 1-1.5°C in severe hypoxia. During prolonged hypoxia, T b stabilized at a new lower temperature. A regulated increase in heat loss contributed to T b depression as reflected by increases in bill surface temperatures (up to 5°C) during hypoxia. Bill warming required peripheral chemoreceptor inputs, since vagotomy abolished this response to hypoxia. T b depression could still occur without bill warming, however, because vagotomized birds reduced T b as much as intact birds. Compared to both greylag geese and pekin ducks, bar-headed geese required more severe hypoxia to initiate T b depression and heat loss from the bill. However, when T b depression or bill warming were expressed relative to arterial O 2 concentration (rather than inspired O 2 ) all species were similar; this suggests that enhanced O 2 loading, rather than differences in thermoregulatory control centres, reduces T b depression during hypoxia in bar-headed geese. Correspondingly, bar-headed geese maintained higher rates of metabolism during severe hypoxia (7% inspired O 2 ), but this was only partly due to differences in T b . Time domains of the hypoxic ventilatory response also appeared to differ between bar-headed geese and low altitude species. Overall, our results suggest that birds can adjust peripheral heat dissipation to facilitate T b depression during hypoxia, and that bar-headed geese minimize T b and metabolic depression as a result of evolutionary adaptations that enhance O 2 transport.

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“…The AVPO has been reported to be an extremely sensitive preoptic region involved in both hypothermia (Barros et al, 2004(Barros et al, , 2006 and fever (Blatteis, 2006;Kwiatkoski et al, 2013). In agreement with this notion, a previous study has suggested that NO in the AVPO is involved in thermoregulatory responses during hypoxic conditions .…”

Section: Discussionsupporting

confidence: 52%

“…Estudos relatam que a AVPO é uma região extremamente sensível envolvida nas fases termorregulatórias de hipotermia (BARROS et al, 2004;BARROS et al, 2006; 35 GARGAGLIONE et al, 2005; e febre (BLATTEIS, 2006;KWIATKOSKI et al, 2013). De acordo com este conceito, um estudo prévio sugeriu que o óxido nítrico (NO) na AVPO também está envolvido nas respostas termorregulatórias durante condições de hipóxia .…”

Section: Efeito Da Administração De Aoa Na Avpo Na Produção De Citocunclassified

Sulfeto de hidrogênio durante o choque endotoxêmico: modulação da produção de PGD<sub>2</sub> na AVPO e de citocinas periféricas durante as fases de hipotermia e febre

Fernández¹

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Orientador: Prof. Dr. Luiz Guilherme de Siqueira Branco. Ribeirão Preto 2017Autorizo a reprodução e divulgação total ou parcial deste trabalho, por qualquer meio convencional ou eletrônico, para fins de estudo e pesquisa, desde que citada a fonte. À meu orientador, Prof Dr Luiz Guilherme Branco, por todo o compromiso, dedicação, conhecimento, paciência e apoio.À minha familia que sempre é um estímulo, um apoio e uma fonte de inspiração na minha formação.À Faculdade de Medicina de Riberão Preto, seu corpo docente, seu pessoal administrativo e não docente, por ter me acolhido e ajudado.À Heloísa Della Coleta Francescato, por ser a melhor colaboradora, companheira e amiga neste processo; também pelo seu conhecimento, paciência e carinho.À Renato Neri Soriano, Glauce Do Nascimento, João Paulo Sabino, Clarissa Mota, Bruna Maitan, Flavia Turcato e Mauro ferreira por serem amigos e irmãos do doutorado que com conhecimento e bons momentos acompanharam todo o processo. As respostas termorregulatórias ao lipopolissacarídeo (LPS) são influenciadas por moduladores que aumentam (febrigênicos) ou diminuem (criogênicos) a temperatura corporal (T b ). Entre eles, o neurotransmissor gasoso sulfeto de hidrogênio (H 2 S) modula a inflamação sistêmica induzida por endotoxina em ratos, agindo como uma molécula anti-inflamatória e criogênica, embora os mecanismos subjacentes ainda sejam pouco compreendidos. Considerando que a endotoxina é um ligante para o receptor Toll-like 4 (TLR4) e que evidências recentes revelam um cross-talk entre a via de sinalização TLR e fosfo-Akt (p-Akt), o objetivo do presente estudo foi investigar se o H 2 S atua como um mediador antiinflamatório e antipirético durante as fases termorregulatórias que ocorrem no choque endotoxêmico (hipotermia e febre) induzido por lipopolissacarídeo bacteriano (LPS, 2,5 mg/kg intraperitoneal (ip)) através da modulação sobre a produção de prostaglandina D 2 (PGD 2 ) e a ativação de Akt na área pré-óptica ântero-ventral do hipotálamo (AVPO). A T b profunda de ratos mantidos a uma temperatura ambiente de 25 °C foi registrada antes e depois da inibição farmacológica da enzima cistationina β-sintase (CBS -responsável pela produção endógena de H 2 S no cérebro) usando aminooxiacetato (AOA, 100 pmol/1 μl intracerebroventricular (icv)), combinado ou não com a administração de LPS. Para esclarecer os mecanismos responsáveis por esses ajustes da resposta imune, foram determinados na AVPO os níveis de H 2 S, a produção de PGD 2 e o perfil de expressão das proteínas CBS, pAkt e p-CREB. Além disso, foi analisada a concentração de citocinas plasmáticas (IL-1β, IL-6, IL-10, TNFα, IFN-γ e IL-4). A injeção ip de LPS causou a hipotermia típica seguida de febre. A microinjeção icv de AOA não causou nenhuma alteração na T b nem na produção basal de PGD 2 durante a eutermia. Os níveis de H 2 S na AVPO aumentaram significativamente durante a hipotermia quando comparado com ratos eutérmicos e febris. Em ratos tratados com LPS, o AOA causou uma atenuação na queda da T b durante a fase de hipote...

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Respiratory and body temperature modulation by adenosine A1 receptors in the anteroventral preoptic region during normoxia and hypoxia

Cited by 37 publications

References 41 publications

Physiological roles of A₁ and A_2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine

Physiological roles of A₁ and A_2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine

Body temperature depression and peripheral heat loss accompany the metabolic and ventilatory responses to hypoxia in low and high altitude birds

Sulfeto de hidrogênio durante o choque endotoxêmico: modulação da produção de PGD<sub>2</sub> na AVPO e de citocinas periféricas durante as fases de hipotermia e febre

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