Davidheiser S
Am J Physiol. 1986 Jul;251(1 Pt 1):C72-7. doi: 10.1152/ajpcell.1986.251.1.C72.
The effects of norepinephrine (NE) and K+ stimulation on aerobic glycolysis (JLac), O2 utilization (JO2), and isometric force of isolated rat anococcygeus smooth muscle were investigated to determine the relationship between metabolism and contractility. A large sustained increase in JLac was measured during NE stimulation, but only a small rise in JLac occurred during high-KCl depolarization. JO2, in both cases, correlated with the force response. The difference in JLac could not be explained solely on the lower force output of K+-depolarized muscles or on increased glycogenolysis during NE stimulation, but was perhaps due to activation of energy-requiring processes associated with receptor- rather than depolarization-mediated Ca2+ mobilization. When muscles were stimulated with a K2SO4 (substituted for NaCl) Krebs-Ringer bicarbonate (KRB) rather than a N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium, JLac was significantly elevated due to an increased intracellular pH as a result of the low external Cl-. Lowering the pH of KRB or adding the anion exchange inhibitor 4-4'-diisothiocyanostilbene-2,2'disulfonic acid prevented the rise in JLac and also restored the initial fast component of the force response to NE in Cl(-)-free solution.
研究了去甲肾上腺素(NE)和钾离子(K⁺)刺激对离体大鼠肛门尾骨肌平滑肌有氧糖酵解(JLac)、氧气利用(JO₂)和等长力的影响,以确定代谢与收缩性之间的关系。在NE刺激期间,测量到JLac有大幅度持续增加,但在高氯化钾去极化期间,JLac仅出现小幅上升。在这两种情况下,JO₂均与力反应相关。JLac的差异不能仅通过K⁺去极化肌肉较低的力输出或NE刺激期间糖原分解增加来解释,可能是由于与受体介导而非去极化介导的Ca²⁺动员相关的耗能过程的激活。当用硫酸钾(代替氯化钠)的碳酸氢盐克氏液(KRB)而非N-2-羟乙基哌嗪-N'-2-乙磺酸缓冲液刺激肌肉时,由于低细胞外氯离子导致细胞内pH升高,JLac显著升高。降低KRB的pH值或添加阴离子交换抑制剂4,4'-二异硫氰酸芪-2,2'-二磺酸可防止JLac升高,并在无氯离子溶液中恢复对NE的力反应的初始快速成分。