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目的:探讨脑动脉平滑肌细胞电压依赖性钙通道(voltage-dependent calcium channels,VDCCs)所介导的尼非地平不敏感电流(nifedipine-insensitive calcium currents,NICCs)与细胞外液二价载荷阳离子的种类和浓度之间的关系。方法:酶促消化法急性分离大鼠脑动脉平滑肌细胞,运用膜片钳研究其在不同二价载荷阳离子细胞外液中的VDCCs电流密度以及对L-VDCCs阻滞剂尼非地平(Nifedipine)和地尔硫卓(Diltiazem)的反应。结果:NICCs存在于以10 mmol/L Ba2+作为二价载荷阳离子的细胞外液中,加入100μmol/L Ca2+后所有VDCCs电流均对尼非地平非敏感;以2 mmol/L的Ba2+或2 mmol/L的Ca2+作为二价载荷阳离子时VDCCs电流均对尼非地平敏感;10 mmol/L的Ba2+中的NICCs可被100μmol/L地尔硫卓完全抑制,由于地尔硫卓对L-VDCCs具有高特异性,故认为NICCs仍是L-VDCCs电流的一部分。结论:再次证实了脑动脉平滑肌细胞仅表达L-型VDCCs,排除了其它类型VDCCs作为脑血流调节或脑血管疾病治疗靶点的潜在可能。
OBJECTIVE: To investigate the effects of nifedipine-insensitive calcium currents (NICCs) mediated by voltage-dependent calcium channels (VDCCs) of cerebral artery smooth muscle cells on the bivalent cationic charge of extracellular fluid And the relationship between concentration. Methods: Rat cerebral artery smooth muscle cells were isolated by enzymatic digestion. The current density of VDCCs in different bivalent loaded cationic extracellular fluids was measured by patch-clamp technique. The effects of Lif-VDCCs blockers such as Nifedipine and Diltiazem reaction. RESULTS: NICCs were present in extracellular fluid containing 10 mmol / L Ba2 + as bivalent cationic charge. All VDCCs currents were non-sensitive to nimodipine after addition of 100 μmol / L Ca2 +; 2 mmol / L Ba2 + or 2 mmol / L and Ca2 + as bivalent loading cation were all sensitive to nifedipine. NICCs in 10 mmol / L Ba2 + were completely inhibited by 100 μmol / L diltiazem. Because diltiazem had high specificity for L-VDCCs, it was considered that NICCs It is still part of the L-VDCCs current. CONCLUSIONS: This demonstrates once again that L-type VDCCs are expressed only in smooth muscle cells of the cerebral artery and preclude the potential of other types of VDCCs as therapeutic targets for cerebral blood flow regulation or cerebrovascular disease.