Azari J, Huxtable R J
Eur J Pharmacol. 1980 Feb 8;61(3):217-23. doi: 10.1016/0014-2999(80)90123-5.
The mechanism of isoproterenol-stimulated taurine uptake was examined in the perfused rat heart. Hearts were perfused by the Langendorff technique in a non-recirculating system, while heart rate and contractile force were determined continuously. Perfusion with inotropic concentrations of glucagon stimulated the uptake of [3H]taurine. If the positive inotropic response to isoproterenol was blocked with verapamil, a calcium antagonist, the uptake of taurine was still stimulated. This indicates that inotropy per se, or calcium influx are not involved in the modulation of taurine influx, but that influx rats is responding to cell cyclic AMP levels. The lack of effect of the positively inotropic ionophores monensin and A23187 and the negatively inotropic ionophore valinomycin is in agreement with this conclusion. Taurine decreased calcium binding to cardiac sarcolemma by 31% at 1 mM concentration and 80% at 5 mM.
在灌注大鼠心脏中研究了异丙肾上腺素刺激牛磺酸摄取的机制。心脏采用Langendorff技术在非循环系统中进行灌注，同时连续测定心率和收缩力。用变力浓度的胰高血糖素灌注可刺激[3H]牛磺酸的摄取。如果用钙拮抗剂维拉帕米阻断对异丙肾上腺素的正性变力反应，牛磺酸的摄取仍会受到刺激。这表明变力作用本身或钙内流不参与牛磺酸内流的调节，而是大鼠内流对细胞环磷酸腺苷水平有反应。正性变力离子载体莫能菌素和A23187以及负性变力离子载体缬氨霉素缺乏作用与该结论一致。牛磺酸在1 mM浓度时可使钙与心肌肌膜的结合减少31%，在5 mM浓度时减少80%。
