Ernsberger P
Department of Nutrition, Case Western Reserve University School of Medicine Cleveland, OH 44106-4906, USA.
J Auton Nerv Syst. 1998 Oct 15;72(2-3):147-54. doi: 10.1016/s0165-1838(98)00099-x.
Rat PC 12 pheochromocytoma cells lack alpha2-adrenergic receptors but express plasma membrane I1-imidazoline receptors. In response to the I1-agonist moxonidine, diglycerides are generated via phosphatidylcholine-selective phospholipase C, and prostaglandin E2 is released. This report characterizes I-receptor-mediated release of arachidonic acid, the precursor to the prostaglandins. PC12 cells were incubated with [3H]arachidonic acid for 24 h and superfused with 0.01% bovine serum albumin in Krebs' physiological buffer at 1 ml/min. Calcium ionophore increased arachidonic acid release only marginally, implying that in PC12 cells arachidonic acid release is not driven by calcium. The I1-agonist moxonidine at concentrations between 10 nM and 1.0 microM rapidly elicited up to two-fold increases in [3H]arachidonic acid release. Guanabenz, a potent alpha2-agonist and I2-ligand, had no effect. The selective I1-antagonist efaroxan blocked the action of moxonidine. The phospholipase A2 inhibitor aristolochic acid had no effect, suggesting that arachidonic acid release may be through an indirect pathway, possibly involving diglycerides. Thus, I1-imidazoline receptors in PC12 cells are coupled to arachidonic acid release through an as yet unknown pathway.
大鼠嗜铬细胞瘤PC12细胞缺乏α2 - 肾上腺素能受体，但表达质膜I1 - 咪唑啉受体。在I1 - 激动剂莫索尼定的作用下，通过磷脂酰胆碱选择性磷脂酶C产生甘油二酯，并释放前列腺素E2。本报告描述了I - 受体介导的花生四烯酸释放，花生四烯酸是前列腺素的前体。将PC12细胞与[3H]花生四烯酸孵育24小时，然后在Krebs生理缓冲液中以1 ml/分钟的速度用0.01%牛血清白蛋白进行灌流。钙离子载体仅略微增加了花生四烯酸的释放，这意味着在PC12细胞中花生四烯酸的释放不是由钙驱动的。浓度在10 nM至1.0 μM之间的I1 - 激动剂莫索尼定迅速引起[3H]花生四烯酸释放增加高达两倍。强效α2 - 激动剂和I2 - 配体胍那苄没有作用。选择性I1 - 拮抗剂依酚氯铵阻断了莫索尼定的作用。磷脂酶A2抑制剂马兜铃酸没有作用，这表明花生四烯酸的释放可能通过间接途径，可能涉及甘油二酯。因此，PC12细胞中的I1 - 咪唑啉受体通过一条尚未明确的途径与花生四烯酸释放偶联。
