Activation of kinin B1 receptor evokes hyperthermia through a vagal sensory mechanism in the rat.
Activation of kinin B1 receptor evokes hyperthermia through a vagal sensory mechanism in the rat.
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DOI：
10.1186/1742-2094-9-214
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发表时间：
2012-09-13
影响因子：
9.3
通讯作者：
Couture R
中科院分区：
文献类型：
--
作者：
Talbot S;De Brito Gariépy H;Saint-Denis J;Couture R
激肽是疼痛和炎症的介质。然而，它们在体温调节中的作用是未知的，尽管B1受体（B1 R）被发现与脂多糖（LPS）诱导的发热有关。本研究的目的是研究外周B1 R影响大鼠模型的身体核心温度的机制，该模型已知显示B1 R水平上调。雄性Sprague-Dawley大鼠接受链脲佐菌素（STZ，65 mg/kg; i. p.）增强B1 R的表达。对照组大鼠仅接受溶媒。一周后，在腹膜内注射递增剂量（0.01至5 mg/kg）的des-Arg 9-缓激肽（BK）和Sar-[D-Phe 8] des-Arg 9-BK（B1 R激动剂）或BK（B2 R激动剂）后，测量清醒大鼠的直肠温度。B1 R诱导的体温过高的机制，解决了使用特定的抑制剂，并在大鼠进行皮下迷走神经结扎。采用实时定量真实的时间聚合酶链反应（qRT-PCR）检测B1 R mRNA水平，并采用共聚焦显微镜进行B1 R定位。B1受体激动剂（0.1至5 mg/kg）在STZ处理大鼠中显示出短暂（5至30分钟）和剂量依赖性的直肠温度升高（+1.5 ° C），但在对照大鼠中没有。BK对STZ和对照组大鼠无影响。在STZ处理的大鼠中，B1 R激动剂诱导的体温升高被B1 R（SSR 240612）、环氧合酶-2（考克斯-2）（尼氟灭酸）和一氧化氮合酶（NOS）（L-NAME）的拮抗剂/抑制剂阻断，并且在迷走神经结扎后。相反，考克斯-1抑制剂（吲哚美辛）对B1受体激动剂诱导的体温升高没有影响。在STZ治疗的大鼠，B1受体mRNA显着增加，在下丘脑和迷走神经，它是共同定位与降钙素基因相关肽的感觉C-纤维。炎症性疾病中诱导的B1 R可通过迷走神经感觉机制参与体温过高，其中迷走神经感觉机制涉及野牡丹素（通过考克斯-2）和一氧化氮。
Kinins are mediators of pain and inflammation. Their role in thermoregulation is, however, unknown despite the fact the B1 receptor (B1R) was found implicated in lipopolysaccharide (LPS)-induced fever. The aim of this study was to investigate the mechanism by which peripheral B1R affects body core temperature in a rat model known to show up-regulated levels of B1R. Male Sprague–Dawley rats received streptozotocin (STZ, 65 mg/kg; i.p.) to enhance B1R expression. Control rats received the vehicle only. One week later, rectal temperature was measured in awake rats after i.p. injection of increasing doses (0.01 to 5 mg/kg) of des-Arg9-Bradykinin (BK) and Sar-[D-Phe8]des-Arg9-BK (B1R agonists) or BK (B2R agonist). The mechanism of B1R-induced hyperthermia was addressed using specific inhibitors and in rats subjected to subdiaphragmatic vagal nerve ligation. B1R mRNA level was measured by quantitative Real Time-polymerase chain reaction (qRT-PCR) and B1R was localized by confocal microscopy. B1R agonists (0.1 to 5 mg/kg) showed transient (5- to 30-minute) and dose-dependent increases of rectal temperature (+1.5°C) in STZ-treated rats, but not in control rats. BK caused no effect in STZ and control rats. In STZ-treated rats, B1R agonist-induced hyperthermia was blocked by antagonists/inhibitors of B1R (SSR240612), cyclooxygenase-2 (COX-2) (niflumic acid) and nitric oxide synthase (NOS) (L-NAME), and after vagal nerve ligation. In contrast, COX-1 inhibition (indomethacin) had no effect on B1R agonist-induced hyperthermia. In STZ-treated rats, B1R mRNA was significantly increased in the hypothalamus and the vagus nerve where it was co-localized with calcitonin-gene-related peptide in sensory C-fibers. B1R, which is induced in inflammatory diseases, could contribute to hyperthermia through a vagal sensory mechanism involving prostaglandins (via COX-2) and nitric oxide.
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影响因子：
5
作者：
Campos, MM;Cabrini, DA;Calixto, JB
通讯作者：
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影响因子：
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作者：
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DOI：
10.1152/ajpgi.1999.276.4.g1052
发表时间：
1999-04-01
影响因子：
4.5
作者：
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通讯作者：
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