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白蛋白致敏和激发豚鼠对气管平滑肌中异丙肾上腺素摄取₂的影响。

Effects of albumin sensitization and challenge of guinea pigs on uptake2 of isoprenaline in trachealis muscle.

作者信息

Bryan-Lluka L J, Vuocolo H E

机构信息

Department of Physiology and Pharmacology, University of Queensland, Brisbane, Australia.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1994 Jun;349(6):578-82. doi: 10.1007/BF01258462.

Abstract

There is evidence that hyperpolarization of cells by various mechanisms results in stimulation of uptake2 of catecholamines and, conversely, that depolarization causes inhibition of uptake2. The aim of this study was to examine whether changes that have been shown to occur in the resting membrane potential of the trachealis muscle of guinea pigs that have been sensitized to albumin (hyperpolarization) or albumin-sensitized followed by inhalational albumin challenge (depolarization) are reflected in changes in uptake2 in the smooth muscle. Uptake2 of isoprenaline (as measured by the steady-state rate of specific 3H-O-methylisoprenaline formation normalized for the isoprenaline concentration) was determined in isolated segments of trachealis muscle that were incubated in 3H-(+/-)-isoprenaline and were from guinea pigs from three treatment groups: (i) controls, (ii) albumin-sensitized and (iii) albumin-sensitized and challenged. At an isoprenaline concentration that does not hyperpolarize the trachealis muscle (1 nmol/l), uptake2 was significantly greater in the muscle from sensitized guinea pigs than that from control or sensitized and challenged guinea pigs. When a drug that hyperpolarized the trachealis muscle was present (25 nmol/l isoprenaline or 10 mumol/l (-)-cromakalim), there were no differences in uptake2 between the three groups. Propranolol prevented the stimulation of uptake2 by isoprenaline and glibenclamide prevented stimulation of uptake2 by (-)-cromakalim. In the presence of propranolol or glibenclamide, there were no differences in uptake2 between the three treatment groups of guinea pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

有证据表明,通过各种机制使细胞超极化会导致儿茶酚胺摄取2增加,相反,去极化会导致摄取2受到抑制。本研究的目的是检查在对白蛋白致敏(超极化)的豚鼠气管平滑肌静息膜电位中已显示发生的变化,或在白蛋白致敏后进行吸入性白蛋白激发(去极化)时,这些变化是否反映在平滑肌摄取2的变化中。在来自三个治疗组的豚鼠的气管肌分离段中测定异丙肾上腺素的摄取2(通过针对异丙肾上腺素浓度标准化的特定3H-O-甲基异丙肾上腺素形成的稳态速率来测量),这些分离段在3H-(+/-)-异丙肾上腺素中孵育:(i)对照组,(ii)白蛋白致敏组和(iii)白蛋白致敏并激发组。在不会使气管肌超极化的异丙肾上腺素浓度(1 nmol/l)下,致敏豚鼠肌肉中的摄取2显著高于对照组或致敏并激发组的豚鼠。当存在使气管肌超极化的药物时(25 nmol/l异丙肾上腺素或10 μmol/l(-)-克罗卡林),三组之间的摄取2没有差异。普萘洛尔可阻止异丙肾上腺素对摄取2的刺激,格列本脲可阻止(-)-克罗卡林对摄取2的刺激。在普萘洛尔或格列本脲存在的情况下,三组豚鼠的摄取2没有差异。(摘要截短为250字)

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