Bülow A
Department of Physiology, University of Göteborg, Sweden.
Acta Physiol Scand. 1996 Aug;157(4):419-26. doi: 10.1046/j.1365-201X.1996.514269000.x.
Myogenic tone and reactivity were studied in isolated, cannulated and pressurized small branches of the femoral artery of the rat. Myogenic tone developed spontaneously under control conditions (1.5 mM Ca2+), reducing the diameter at 80 mmHg to 64 +/- 6% of the 'max 80', i.e. the diameter in Ca2+ free solution, which was 221 +/- 23 microns (mean +/- SD, n = 18). The calcium channel blockers verapamil and diltiazem, dose-dependently, decreased this myogenic tone with pIC50 values of 6.9 +/- 0.2 (n = 7) and 6.6 +/- 0.1 (n = 6), respectively. Myogenic reactivity was demonstrated under control conditions as a sustained decrease in diameter, by 5 +/- 3% of max 80 (after an initial, transient distension), in response to a step increase in transmural pressure from 80 to 140 mmHg. This response to the pressure increase was markedly inhibited when myogenic tone had been reduced by 50% with verapamil or diltiazem resulting, in fact, in an increased steady state diameter by 2 +/- 1 and 1 +/- 1% at 140 compared with 80 mmHg. However, if myogenic tone was reduced to the same extent by low extracellular Ca2+ (approximately 0.3 mM) the vessels constricted by 6 +/- 1% in response to the pressure increase, an effect comparable to that in control Ca2+. Moreover, 50% reductions in myogenic tone by ACh (approximately 0.1 microM) or pinacidil (approximately 0.3 microM) were associated with significantly enhanced reactivity; steady state diameter decreased by as much as 11 +/- 4 and 15 +/- 5% of max 80. These results suggest that voltage dependent L-type Ca2+ channels are involved both in myogenic tone and in the myogenic response to a rise in vascular transmural pressure in skeletal muscle arteries. Partial inhibition of myogenic tone by other pharmacological routes do not necessarily interfere with myogenic reactivity since the response was, in fact, enhanced in the presence of ACh or pinacidil.
在大鼠股动脉分离、插管并加压的小分支中研究了肌源性张力和反应性。在对照条件下（1.5 mM Ca2+），肌源性张力自发产生，将80 mmHg时的直径降低至“最大80”的64±6%，即无Ca2+溶液中的直径，其为221±23微米（平均值±标准差，n = 18）。钙通道阻滞剂维拉帕米和地尔硫卓剂量依赖性地降低这种肌源性张力，pIC50值分别为6.9±0.2（n = 7）和6.6±0.1（n = 6）。在对照条件下，肌源性反应性表现为直径持续减小，在跨壁压力从80 mmHg逐步增加到140 mmHg后，直径减小至最大80的5±3%（初始短暂扩张后）。当用维拉帕米或地尔硫卓将肌源性张力降低50%时，对压力增加的这种反应明显受到抑制，实际上，与80 mmHg相比，在140 mmHg时稳态直径增加了2±1%和1±1%。然而，如果通过低细胞外Ca2+（约0.3 mM）将肌源性张力降低到相同程度，血管在压力增加时收缩6±1%，这一效应与对照Ca2+条件下相当。此外，乙酰胆碱（约0.1 microM）或匹那地尔（约0.3 microM）使肌源性张力降低50%与反应性显著增强相关；稳态直径分别减小至最大80的11±4%和15±5%。这些结果表明，电压依赖性L型Ca2+通道参与了骨骼肌动脉的肌源性张力以及对血管跨壁压力升高的肌源性反应。通过其他药理学途径对肌源性张力的部分抑制不一定会干扰肌源性反应性，因为在乙酰胆碱或匹那地尔存在的情况下，反应实际上增强了。
