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儿茶酚胺诱导小鼠外翻肠囊水分转运的代谢基础

Metabolic basis of catecholamine-induced water transport in everted gut sacs of mouse.

作者信息

Mary P L, Rao J P

机构信息

Department of Physiology, Christian Medical College, Vellore, India.

出版信息

Clin Exp Pharmacol Physiol. 1991 Jul;18(7):483-8. doi: 10.1111/j.1440-1681.1991.tb01481.x.

DOI:10.1111/j.1440-1681.1991.tb01481.x
PMID:1914249
Abstract
  1. Catecholamine-induced water transport was measured using an everted gut sac technique. Adrenaline, noradrenaline and isoprenaline induce dose-dependent increases in water transport by the proximal intestinal sacs. Use of selective adrenergic agents revealed the possible involvement of alpha 1- and beta 2-receptors in mediation of catecholamine stimulation of water transport in this segment. 2. Inhibition of glycolysis reduced the effect mediated through alpha 1-receptors, while the inhibition of oxidative phosphorylation blocked the beta 2-receptor mediated increase in water transport. 3. Basal transport of water was also significantly reduced by inhibition of glycolysis but was significantly elevated by blockage of oxidative phosphorylation. 4. Suppression or stimulation of glycolysis was paralleled by similar changes in lactic acid release from the gut wall. 5. It is concluded that the energy for the catecholamine-induced water transport is contributed by glycolysis and oxidative phosphorylation coupled to alpha 1- and beta 2-receptors, respectively. Under basal conditions water transport is mainly dependent on glycolysis in the segment of intestine examined.
摘要
  1. 采用外翻肠囊技术测定儿茶酚胺诱导的水转运。肾上腺素、去甲肾上腺素和异丙肾上腺素可使近端肠囊的水转运呈剂量依赖性增加。使用选择性肾上腺素能药物表明,α1和β2受体可能参与介导该节段儿茶酚胺刺激的水转运。2. 糖酵解的抑制降低了通过α1受体介导的效应,而氧化磷酸化的抑制则阻断了β2受体介导的水转运增加。3. 糖酵解的抑制也显著降低了基础水转运,但氧化磷酸化的阻断则使其显著升高。4. 糖酵解的抑制或刺激伴随着肠壁乳酸释放的类似变化。5. 得出的结论是,儿茶酚胺诱导的水转运能量分别由与α1和β2受体偶联的糖酵解和氧化磷酸化提供。在基础条件下,在所检查的肠段中,水转运主要依赖于糖酵解。

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