cAMP-mediated regulation of chloride secretion by the opercular epithelium.
cAMP-mediated regulation of chloride secretion by the opercular epithelium.
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cAMP 介导的岛盖上皮氯分泌调节。
DOI：
10.1152/ajpregu.1984.246.5.r741
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
K. Degnan
中科院分区：
文献类型：
--
作者：
S. A. May;K. Degnan
用3-异丁基-1-甲基黄嘌呤(IBMX)、福司可林和肾上腺素能激动剂研究儿茶酚胺对眼盖上皮细胞氯离子分泌速率(短路电流)和环磷酸腺苷(CAMP)水平的调节作用。在这个组织中，α-肾上腺素能激动剂抑制ISC，而β-肾上腺素能激动剂刺激ISC(J.Physiol.伦敦294：483-495,1979)。IBMX和Forsklin分别刺激ISC125和85%，同时使cAMP水平分别升高2.5倍和70.0倍。这些发现证实了先前的观察结果，即该组织中ISC的刺激是由cAMP升高所介导的(J.comp.物理。B145：29-35,1981)。异丙肾上腺素是一种β-激动剂，对IBMX或Forsklin刺激的组织的ISC没有影响，但使IBMX刺激的组织的cAMP水平增加了5.8倍。α-激动剂可乐定仅抑制IBMX刺激的组织中的ISC，对IBMX或Forsklin刺激的组织中的cAMP水平没有影响。这些发现表明，当cAMP水平保持升高时，儿茶酚胺对ISC的抑制作用可以发生，这表明这种作用不是通过降低cAMP水平来调节的。这一观察结果有力地证明了儿茶酚胺抑制眼盖上皮和类似上皮的氯离子分泌的cAMP非依赖性机制。
Catecholamine regulation of the Cl- secretion rate (short-circuit current, Isc) and adenosine 3',5'-cyclic monophosphate (cAMP) levels of the opercular epithelium was investigated by using 3-isobutyl-1-methylxanthine (IBMX), forskolin, and adrenergic agonists. In this tissue alpha-adrenergic agonists inhibit, and beta-adrenergic agonists stimulate, the Isc (J. Physiol. London 294: 483-495, 1979). IBMX and forskolin stimulated the Isc 125 and 85%, respectively, and simultaneously produced 2.5- and 70.0-fold elevations in the cAMP levels, respectively. These findings confirm previous observations demonstrating that stimulation of the Isc in this tissue is mediated by elevations in cAMP (J. Comp. Physiol. B 145: 29-35, 1981). Isoproterenol, a beta-agonist, had no effect on the Isc of either IBMX- or forskolin-stimulated tissues but increased the cAMP level an additional 5.8-fold in IBMX-stimulated tissues. Clonidine, an alpha-agonist, inhibited the Isc in IBMX-stimulated tissues only and had no effect on cAMP levels in either IBMX- or forskolin-stimulated tissues. These findings demonstrate that catecholamine-induced inhibition of the Isc can occur while the cAMP level remains elevated, indicating that this effect is not mediated by lowering cAMP levels. This observation is strong evidence for a cAMP-independent mechanism for catecholamine-induced inhibition of Cl- secretion in the opercular and similar epithelia.