Wesselman J P, VanBavel E, Pfaffendorf M, Spaan J A
Department of Medical Physics, University of Amsterdam, Netherlands.
J Vasc Res. 1996 Jan-Feb;33(1):32-41. doi: 10.1159/000159129.
The role of L-type voltage-operated Ca2+ channels (VOCs) in myogenic responsiveness was studied in cannulated rat mesenteric small arteries [mean diameter at 100 mm Hg and full dilation was 329 +/- 9 (SE) micrometer]. Twenty-six arteries were cannulated and pressurized. The luminal cross-sectional area of these vessels was monitored continuously. To test for myogenic responsiveness, pressure was raised stepwise from 20 to 60 and from 60 to 100 mm Hg. Pressure elevation enhanced the vascular tone, reflecting spontaneous myogenic responsiveness. Nifedipine (1 and 10 microM) suppressed spontaneous myogenic responses. The alpha1-adrenoceptor agonist phenylephrine (1 and 10 microM), when administered at 20 mm Hg, elicited constriction and vasomotion, and potentiated myogenic constriction to subsequent pressure elevation. Nifedipine (1 and 10 microM) also suppressed phenylephrine-potentiated myogenic responsiveness. Stimulation of VOCs with BAY K 8644 (10-300 nM) had no effect at 20 mm Hg, but augmented myogenic responsiveness. K+ (16-46 mM) caused concentration-dependent constrictions when administered at 20 mm Hg, and potentiated myogenic responsiveness when the pressure was raised from 20 to 60 mm Hg. Thus, any intervention that blocked the VOCs also blocked myogenic responses. Therefore, we conclude that VOCs are essential for the myogenic responsiveness of cannulated rat mesenteric small arteries.
在插管的大鼠肠系膜小动脉[100 mmHg时的平均直径和完全扩张时为329±9（标准误）微米]中研究了L型电压门控Ca2+通道（VOCs）在肌源性反应性中的作用。26条动脉被插管并加压。连续监测这些血管的管腔横截面积。为了测试肌源性反应性，压力从20 mmHg逐步升至60 mmHg，再从60 mmHg升至100 mmHg。压力升高增强了血管张力，反映出自发性肌源性反应性。硝苯地平（1和10 μM）抑制自发性肌源性反应。α1肾上腺素能受体激动剂去氧肾上腺素（1和10 μM）在20 mmHg时给药，可引起收缩和血管运动，并增强对随后压力升高的肌源性收缩。硝苯地平（1和10 μM）也抑制去氧肾上腺素增强后的肌源性反应性。用BAY K 8644（10 - 300 nM）刺激VOCs在20 mmHg时无作用，但增强了肌源性反应性。K+（16 - 46 mM）在20 mmHg时给药引起浓度依赖性收缩，当压力从20 mmHg升至60 mmHg时增强肌源性反应性。因此，任何阻断VOCs的干预也会阻断肌源性反应。所以，我们得出结论，VOCs对于插管大鼠肠系膜小动脉的肌源性反应性至关重要。
