Liedtke C M
Department of Pediatrics, Rainbow Babies and Children Hospital, Cleveland, Ohio.
Am J Physiol. 1992 May;262(5 Pt 1):L621-7. doi: 10.1152/ajplung.1992.262.5.L621.
Loop diuretic-sensitive NaCl(K) cotransport plays a fundamental role in absorption and secretion of electrolytes in epithelial tissues. Cotransport activity was measured as uptake of 22Na, 36Cl, or 86Rb at 27 degrees C in isolated rabbit tracheal epithelial cells. Uptake of radiotracer was linear from 1 to 2 min after initiation of radiotracer transport. Bumetanide at 10 microM final concentration did not affect tracer uptake. The endogenous catecholamine l-epinephrine and alpha 2-adrenergic agent clonidine increased sodium and chloride uptake at least 5.5-fold. Bumetanide blocked sodium uptake by 85% and chloride uptake by 72%. 86Rb uptake was not affected by l-epinephrine, clonidine, or bumetanide. The alpha 2-adrenergic antagonist yohimbine blocked the effects of l-epinephrine and clonidine on 22Na and 36Cl uptake. In Ca(2+)-depleted transport medium, baseline levels of sodium and chloride uptake increased 3.8- and 2.4-fold, respectively, in a bumetanide-independent manner. Nevertheless, l-epinephrine and clonidine induced a net stimulation of sodium and chloride uptake similar to that found in Ca(2+)-replete medium. This response was reduced by bumetanide and yohimbine. The Ca(2+)-elevating agent ionomycin increased bumetanide-sensitive sodium and chloride uptake 7.2- and 6.2-fold, respectively. Replacement of chloride with gluconate or sodium with N-methyl-D-glucamine in the extracellular medium inhibited l-epinephrine and clonidine-stimulated bumetanide-sensitive sodium and chloride uptake, respectively. Osmotic shrinkage in hyperosmotic (500 mM NaCl with all other electrolytes at normal concentration) transport medium markedly increased bumetanide-inhibitable sodium and chloride uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
袢利尿剂敏感的NaCl(K)共转运在上皮组织电解质的吸收和分泌中起重要作用。共转运活性通过在27℃下测量分离的兔气管上皮细胞对22Na、36Cl或86Rb的摄取来测定。放射性示踪剂转运开始后1至2分钟内，放射性示踪剂的摄取呈线性。终浓度为10 microM的布美他尼不影响示踪剂摄取。内源性儿茶酚胺L-肾上腺素和α2-肾上腺素能药物可乐定使钠和氯的摄取至少增加5.5倍。布美他尼使钠摄取减少85%，氯摄取减少72%。86Rb摄取不受L-肾上腺素、可乐定或布美他尼影响。α2-肾上腺素能拮抗剂育亨宾可阻断L-肾上腺素和可乐定对22Na和36Cl摄取的作用。在无钙的转运培养基中，钠和氯摄取的基线水平分别以不依赖布美他尼的方式增加3.8倍和2.4倍。然而，L-肾上腺素和可乐定对钠和氯摄取仍有净刺激作用，与在含钙充足培养基中发现的情况相似。布美他尼和育亨宾可减弱这种反应。钙升高剂离子霉素使布美他尼敏感的钠和氯摄取分别增加7.2倍和6.2倍。在细胞外培养基中用葡萄糖酸盐替代氯或用N-甲基-D-葡糖胺替代钠，分别抑制L-肾上腺素和可乐定刺激的布美他尼敏感的钠和氯摄取。在高渗(500 mM NaCl，其他所有电解质浓度正常)转运培养基中的渗透性收缩显著增加了布美他尼可抑制的钠和氯摄取。(摘要截选至250字)
