Kim Young Chul, Lee Sang Jin, Kim Ki Whan
Department of Physiology, Chungbuk National University College of Medicine, Cheongju, Korea.
J Korean Med Sci. 2004 Feb;19(1):42-50. doi: 10.3346/jkms.2004.19.1.42.
Effects of pH on vascular tone and L-type Ca2+ channels were investigated using Mulvany myograph and voltage-clamp technique in rabbit basilar arteries. In rabbit basilar arteries, high K+ produced tonic contractions by 11+/-0.6 mN (mean+/-S.E.,n=19). When extracellular pH (pHo) was changed from control 7.4 to 7.9 ([alkalosis]o), K+-induced contraction was increased to 128+/-2.1% of the control (n=13). However, K+-induced contraction was decreased to 73+/-1.3% of the control at pHo 6.8 ([acidosis] o, n=4). Histamine (10 microM) also produced tonic contraction by 11+/-0.6 mN (n=17), which was blocked by post-application of nicardipine (1 microM). [alkalosis]o and [acidosis]o increased or decreased histamine-induced contraction to 134+/-5.7% and 27+/-7.6% of the control (n=4, 6). Since high K+- and histamine-induced tonic contractions were affected by nicardipine and pHo, the effect of pHo on voltage-dependent L-type Ca2+ channel (VDCCL) was studied. VDCCL was modulated by pHo: the peak value of Ca2+ channel current (IBa) at a holding of 0 mV decreased in [acidosis]o by 41+/-8.8%, whereas that increased in [alkalosis]o by 35+/-2.1% (n=3). These results suggested that the external pH regulates vascular tone partly via the modulation of VDCC in rabbit basilar arteries.
采用Mulvany肌张力测定仪和电压钳技术，研究了pH对兔基底动脉血管张力和L型Ca2+通道的影响。在兔基底动脉中，高钾可引起11±0.6 mN（平均值±标准误，n = 19）的强直收缩。当细胞外pH（pHo）从对照值7.4变为7.9（[碱中毒]o）时，钾诱导的收缩增加至对照值的128±2.1%（n = 13）。然而，在pHo为6.8（[酸中毒]o，n = 4）时，钾诱导的收缩减少至对照值的73±1.3%。组胺（10 μM）也可引起11±0.6 mN的强直收缩（n = 17），在应用尼卡地平（1 μM）后该收缩被阻断。[碱中毒]o和[酸中毒]o使组胺诱导的收缩分别增加或减少至对照值的134±5.7%和27±7.6%（n = 4, 6）。由于高钾和组胺诱导的强直收缩受尼卡地平和pHo的影响，因此研究了pHo对电压依赖性L型Ca2+通道（VDCCL）的作用。VDCCL受pHo调节：在0 mV钳制电压下，[酸中毒]o时Ca2+通道电流（IBa）峰值降低41±8.8%，而[碱中毒]o时增加35±2.1%（n = 3）。这些结果表明，细胞外pH通过调节兔基底动脉中的VDCC部分地调节血管张力。
