Shan J J, Li B, Taniguchi N, Pang P K
Department of Physiology, Faculty of Medicine, University of Alberta, Edmonton, Canada.
Steroids. 1996 Nov;61(11):657-63. doi: 10.1016/s0039-128x(96)00186-9.
Pharmacological doses of 24R,25-dihydroxyvitamin D3 (24,25D3) inhibited both phasic and tonic contraction of Sprague-Dawley (SD) rat tail artery helical strips induced by KCl, norepinephrine (NE), and arginine vasopressin (AVP) in organ-bath studies. 24,25D3 also decreased the tension dependent on external calcium influx induced by KCl, AVP, and NE and the tension dependent on internal calcium release from intracellular calcium stores induced by NE. In vascular smooth muscle cells isolated from SD rat tail artery, 24,25D3 reduced membrane L-type calcium channel current and the increment of intracellular calcium concentration induced by KCl. It is suggested that 24,25D3 directly relaxed precontracted SD rat-tail artery by its inhibitory effect on plasma membrane and intracellular organelle calcium channels.
在器官浴研究中，药理剂量的24R,25-二羟基维生素D3（24,25D3）可抑制由氯化钾、去甲肾上腺素（NE）和精氨酸加压素（AVP）诱导的斯普拉格-道利（SD）大鼠尾动脉螺旋条的相性和强直性收缩。24,25D3还降低了由氯化钾、AVP和NE诱导的依赖于细胞外钙内流的张力，以及由NE诱导的依赖于细胞内钙库释放的细胞内钙的张力。在从SD大鼠尾动脉分离的血管平滑肌细胞中，24,25D3降低了细胞膜L型钙通道电流以及由氯化钾诱导的细胞内钙浓度的增加。提示24,25D3通过对质膜和细胞内细胞器钙通道的抑制作用直接舒张预收缩的SD大鼠尾动脉。
