Trujillo Xóchitl, Huerta Miguel, Vásquez Clemente, Andrade Felipa
Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Mexico.
J Muscle Res Cell Motil. 2002;23(2):157-65. doi: 10.1023/a:1020295702288.
The effects of adrenaline and the beta-adrenergic agonist isoprenaline on K+-evoked tension (K+-contracture) and Ba2+ current were investigated in chicken slow (anterior latissimus dorsi (ald)) muscle using isometric-tension measurements and current recording. Addition of adrenaline (10(-7) - 10(-5) M) or isoprenaline (10(-6) - 10(-5) M) to the bath reduced the amplitude of the K+-contractures. These effects were blocked by the beta-antagonist propranolol (5 x 10(-6) M). External application of a cAMP analogue (8-bromo cyclic AMP; 1 x 10(-4) M) also decreased the amplitude of the K+-contractures. To analyze the possible relationship between the induced tension reduction and effects on sarcolemmal Ca2+ channels, a slow action potential and a slow inward membrane current were studied in intact ald chicken muscle fibres. When the ald muscle was immersed in a Na+- and Cl--free solution containing Ba2+ and depolarizing pulses were delivered from a -80 mV holding potential, the muscle fibres exhibited a small, slow Ba2+-dependent potential (observed at about -26 mV, peak amplitude, around -10 mV). The response was blocked by the addition of Co2+ (5 mM) or Cd2+ (2 mM). Using the three-microelectrode voltage-clamp technique, a slow inward membrane current underlying the Ba2+ potential could be discerned. The current had a mean threshold of -60 mV, reached maximum at about -5 mV and ranged from ca. 9 to 19 pA/cm2 (depending on the external Ba2+ concentration). It had a mean reversal potential of +45 mV. The Ba2+ inward current was diminished when adrenaline or isoprenaline was added to the bath (1 x 10(-5) M); however, this decrease did not occur when propranolol was present (5 x 10-6 M). These results suggest that the decreases in the tension of K+-contractures induced by adrenaline and isoprenaline may occur through beta-adrenergic effects on sarcolemmal Ca2+ channels in ald chicken slow muscle fibres.
利用等长张力测量和电流记录技术，研究了肾上腺素和β-肾上腺素能激动剂异丙肾上腺素对鸡慢肌（背阔肌前肌（ald））中钾离子诱发张力（钾离子挛缩）和钡离子电流的影响。向浴液中添加肾上腺素（10⁻⁷ - 10⁻⁵ M）或异丙肾上腺素（10⁻⁶ - 10⁻⁵ M）可降低钾离子挛缩的幅度。这些作用被β-拮抗剂普萘洛尔（5×10⁻⁶ M）阻断。外用环磷酸腺苷类似物（8-溴环磷酸腺苷；1×10⁻⁴ M）也可降低钾离子挛缩的幅度。为了分析诱导的张力降低与对肌膜钙离子通道的影响之间的可能关系，在完整的ald鸡肌纤维中研究了慢动作电位和慢内向膜电流。当ald肌浸入含钡离子的无钠和无氯溶液中，并从 -80 mV的 holding 电位施加去极化脉冲时，肌纤维表现出一个小的、缓慢的钡离子依赖性电位（在约 -26 mV处观察到，峰值幅度约为 -10 mV）。加入钴离子（5 mM）或镉离子（2 mM）可阻断该反应。使用三微电极电压钳技术，可以辨别出钡离子电位背后的慢内向膜电流。该电流的平均阈值为 -60 mV，在约 -5 mV时达到最大值，范围约为9至19 pA/cm²（取决于外部钡离子浓度）。其平均反转电位为 +45 mV。当向浴液中添加肾上腺素或异丙肾上腺素（1×10⁻⁵ M）时，钡离子内向电流减小；然而，当存在普萘洛尔（5×10⁻⁶ M）时，这种减小并未发生。这些结果表明，肾上腺素和异丙肾上腺素诱导的钾离子挛缩张力降低可能是通过β-肾上腺素能对ald鸡慢肌纤维肌膜钙离子通道的作用而发生的。
