Komabayashi T, Tsuboi M
Nihon Seirigaku Zasshi. 1976;38(11):447-56.
This investigation was undertaken to clarify the mechanism of the stimulated--respiration caused by K+ or norepinephrine in brown adipose tissue. 1. The addition of 30 approximately 100 mM K+ stimulated remarkably oxygen uptake in brown adipose tissue, and similarly norepinephrine (0.1 or 1.0 mug/ml) caused a marked stimulation. 2. Even if Na+ in normal Ringer solution was replaced by Choline or Li+, oxygen uptake caused by K+ (30 mM) or norepinephrine (1.0 mug/ml) was unaffected. 3. K+ -induced oxygen uptake was not observed when a Ca2+ -deficient tissue was incubated in Ca2+ -free Ringer, while norepinephrine-induced oxygen uptake clearly observed. And the oxygen uptake of Ca2+ -deficient tissue due to K+ was recovered by the addition of 5 mM Ca2+. 4. Mn2+ (6 mM) or La3+ (10 mM) inhibited significantly oxygen uptake due to K+, but not oxygen uptake due to norepinephrine. 5. K+ -induced oxygen uptake was unaffected by 10(-4) or 10(-3)M ouabain, but norepinephrine-induced oxygen uptake was inhibited considerably by 10(-4)M ouabain. 6. The oxygen uptake due to K+ was unaffected by propranolol (33 muM), whereas that due to norepinephrine was significantly inhibited in the presence of propranolol. 7. In the tissue from reserpine-treated animal, the oxygen uptake caused by K+ was observed. According, from these positive results we are justified to suggest that K+ -induced oxygen uptake is dependent on the presence of Ca2+, and not always caused by catecholamines released secondarily from nerve terminal.
本研究旨在阐明钾离子（K⁺）或去甲肾上腺素在棕色脂肪组织中引起刺激呼吸的机制。1. 添加30至100 mM的K⁺可显著刺激棕色脂肪组织的氧摄取，同样，去甲肾上腺素（0.1或1.0μg/ml）也会引起显著刺激。2. 即使正常林格液中的Na⁺被胆碱或Li⁺取代，K⁺（30 mM）或去甲肾上腺素（1.0μg/ml）引起的氧摄取也不受影响。3. 当将缺钙组织在无钙林格液中孵育时，未观察到K⁺诱导的氧摄取，而去甲肾上腺素诱导的氧摄取则清晰可见。并且，添加5 mM Ca²⁺可使缺钙组织因K⁺引起的氧摄取恢复。4. Mn²⁺（6 mM）或La³⁺（10 mM）显著抑制K⁺引起的氧摄取，但不抑制去甲肾上腺素引起的氧摄取。5. 10⁻⁴或10⁻³M哇巴因不影响K⁺诱导的氧摄取，但10⁻⁴M哇巴因可显著抑制去甲肾上腺素诱导的氧摄取。6. 普萘洛尔（33μM）不影响K⁺引起的氧摄取，而在普萘洛尔存在时，去甲肾上腺素引起的氧摄取则显著受到抑制。7. 在利血平处理动物的组织中，观察到了K⁺引起的氧摄取。因此，基于这些阳性结果，我们有理由认为K⁺诱导的氧摄取依赖于Ca²⁺的存在，并不总是由神经末梢继发性释放的儿茶酚胺引起。
