Gouw M A, Wilffert B, Wermelskirchen D, van Zwieten P A
Division of Pharmacotherapy, University of Amsterdam, The Netherlands.
Pharmacology. 1990;40(5):277-87. doi: 10.1159/000138673.
We determined the contribution of intracellular Ca2+ to the noradrenaline (NA, 3 X 10(-5) mmol/l)-induced contraction of the isolated guinea pig aorta. Since only about 55% of the NA-induced contraction could be attributed to intracellular Ca2+ release, we assumed that a Ca2+ influx component contributes to the NA-induced contraction. This influx component proved resistant to the organic calcium entry blockers (CEBs) nifedipine, diltiazem, flunarizine and gallopamil which, in contrast, antagonized K(+)-induced Ca2+ influx completely. Conversely, the NA-induced Ca2+ influx component could be antagonized by the inorganic cations La3+, Cd2+, Mn2+, Ni2+ and Co2+. 45Ca2+ uptake experiments also revealed that both KCl and NA induce Ca2+ influx of which only the latter one is resistant to nifedipine. It was concluded that in the guinea pig aorta NA activates a receptor-operated channel through which Ca2+ can be translocated from the extracellular space to the cytosol to contribute directly to contraction.
我们测定了细胞内钙离子对去甲肾上腺素（NA，3×10⁻⁵ mmol/L）诱导的离体豚鼠主动脉收缩的作用。由于NA诱导的收缩中只有约55%可归因于细胞内钙离子释放，我们推测钙离子内流成分对NA诱导的收缩有作用。事实证明，这种内流成分对有机钙通道阻滞剂（CEBs）硝苯地平、地尔硫䓬、氟桂利嗪和加洛帕米具有抗性，相比之下，这些阻滞剂能完全拮抗钾离子诱导的钙离子内流。相反，NA诱导的钙离子内流成分可被无机阳离子镧³⁺、镉²⁺、锰²⁺、镍²⁺和钴²⁺拮抗。⁴⁵Ca²⁺摄取实验还表明，氯化钾和NA均可诱导钙离子内流，其中只有后者对硝苯地平具有抗性。得出的结论是，在豚鼠主动脉中，NA激活了一个受体操纵通道，钙离子可通过该通道从细胞外空间转运至细胞质中，直接导致收缩。
