Loutzenhiser R, Epstein M
Eur J Pharmacol. 1984 Oct 30;106(1):47-52. doi: 10.1016/0014-2999(84)90676-9.
The activation of human vascular smooth muscle by KCl-induced depolarization or norepinephrine and the inhibition produced by nitrendipine were studied in the isolated human renal artery. The contractile response of arterial rings to 80 mM KCl was abolished when extracellular Ca2+ was removed, and was inhibited by nitrendipine (IC50 = 10(-8) M). In contrast, a residual, transient contractile response to norepinephrine remained when extracellular Ca2+ was removed and the norepinephrine-induced contractions obtained in the presence of extracellular Ca2+ were not blocked by nitrendipine. KCl caused a stimulation of 45Ca influx which was completely prevented by 10(-6) M nitrendipine. Norepinephrine also caused a stimulation of 45Ca influx; however, the norepinephrine-induced 45Ca influx was not prevented by 10(-6) M nitrendipine. These findings are consistent with the concept that depolarization-induced activation of the human renal artery is primarily dependent upon a stimulation of Ca2+ influx; whereas activation by norepinephrine involves the release of intracellular Ca2+ in addition to the activation of a separate, receptor-operated Ca2+ influx pathway.
在离体人肾动脉中研究了氯化钾诱导的去极化或去甲肾上腺素对人血管平滑肌的激活作用以及尼群地平产生的抑制作用。当去除细胞外钙离子时，动脉环对80 mM氯化钾的收缩反应消失，且被尼群地平抑制（半数抑制浓度=10^(-8) M）。相比之下，去除细胞外钙离子时，对去甲肾上腺素仍存在残余的短暂收缩反应，且细胞外钙离子存在时去甲肾上腺素诱导的收缩未被尼群地平阻断。氯化钾引起45钙内流增加，10^(-6) M尼群地平可完全阻止该作用。去甲肾上腺素也引起45钙内流增加；然而，10^(-6) M尼群地平不能阻止去甲肾上腺素诱导的45钙内流。这些发现与以下概念一致：去极化诱导的人肾动脉激活主要依赖于钙内流的刺激；而去甲肾上腺素激活除了激活一条独立的受体操纵性钙内流途径外，还涉及细胞内钙的释放。
