Endogenous adenosine is an autacoid feedback inhibitor of chloride transport in the shark rectal gland.
Endogenous adenosine is an autacoid feedback inhibitor of chloride transport in the shark rectal gland.
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内源性腺苷是鲨鱼直肠腺中氯离子转运的自体反馈抑制剂。
DOI：
10.1172/jci115517
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
ForrestJr,JN
中科院分区：
文献类型：
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作者：
Kelley,GG;Aassar,OS;ForrestJr,JN
本研究定义了内源性腺苷在灌注鲨鱼直肠腺的生理作用，模型上皮细胞的鲨鱼刺激的氯离子运输。氯离子分泌，静脉腺苷和肌苷浓度增加平行响应激素刺激。从157 +/- 26 μ eq/h/g的基础速率，氯分泌增加到836 +/- 96和2170 +/- 358，使用1和10 μ M毛喉素，静脉腺苷从5.0 +/- 1增加到126 +/- 29和896 +/- 181 nM，肌苷从30 +/- 9增加到349 +/- 77和1719 +/- 454 nM（所有P均小于0.01）。核苷转运抑制剂硝基苄硫代肌苷（NBTI）可完全阻断腺苷和肌苷的释放。布美他尼（Na+/K+/2Cl-协同转运蛋白抑制剂）或哇巴因（Na+/K+ ATP酶活性抑制剂）抑制氯离子转运，使静脉腺苷和肌苷降至基础值。当内源性腺苷与细胞外受体的相互作用被腺苷脱氨酶、NBTI或8-苯基茶碱阻止时，对促分泌素的氯离子转运反应增加了1.7-2.3倍。这些研究表明，内源性腺苷是响应于腺苷酸刺激的细胞工作而释放的，并作为氯离子转运的反馈抑制剂作用于A1腺苷受体。图片
The present studies define the physiologic role of endogenous adenosine in the perfused shark rectal gland, a model epithelia for hormone-stimulated chloride transport. Chloride ion secretion, and venous adenosine and inosine concentrations increased in parallel in response to hormone stimulation. From a basal rate of 157 +/- 26 mu eq/h per g, chloride secretion increased to 836 +/- 96 and 2170 +/- 358 with 1 and 10 microM forskolin, venous adenosine increased from 5.0 +/- 1 to 126 +/- 29 and 896 +/- 181 nM, and inosine increased from 30 +/- 9 to 349 +/- 77 and 1719 +/- 454 nM (all P less than 0.01). Nitrobenzylthioinosine (NBTI), a nucleoside transport inhibitor, completely blocked the release of adenosine and inosine. Inhibition of chloride transport with bumetanide, an inhibitor of the Na+/K+/2Cl- cotransporter, or ouabain, an inhibitor of Na+/K+ ATPase activity, reduced venous adenosine and inosine to basal values. When the interaction of endogenous adenosine with extracellular receptors was prevented by adenosine deaminase, NBTI, or 8-phenyltheophylline, the chloride transport response to secretagogues increased by 1.7-2.3-fold. These studies demonstrate that endogenous adenosine is released in response to hormone-stimulated cellular work and acts at A1 adenosine receptors as a feedback inhibitor of chloride transport.Images