Xu J, Qu Z X, Moore S A, Hsu C Y, Hogan E L
Department of Neurology, Medical University of South Carolina, Charleston 29425.
J Neurochem. 1992 May;58(5):1930-5. doi: 10.1111/j.1471-4159.1992.tb10071.x.
The receptor agonist-mediated hydrolysis of phosphoinositides and production of prostacyclin were studied in murine cerebral endothelial cells (MCEC). Of 11 neurotransmitters and neuromodulators examined, carbachol, noradrenaline (NE), bradykinin, and thrombin significantly increased 3H-inositol phosphate accumulation in the presence of LiCl (20 mM). The maximal stimulation of [3H]inositol monophosphate ([3H]IP1) reached approximately 11, 11, seven, and four times the basal levels for carbachol, NE, bradykinin, and thrombin, respectively. The EC50 values of IP1 accumulation for carbachol and NE were 34 and 0.16 microM, respectively. The muscarinic antagonists, atropine and pirenzepine, blocked the carbachol-induced IP1 accumulation with Ki values of 0.3 and 30 nM, respectively. The adrenergic antagonist, prazosin, blocked NE-induced IP1 accumulation with a Ki of 0.1 nM. The calcium ionophore A23187, histamine, glutamate, vasopressin, serotonin, platelet activating factor, and substance P did not stimulate IP1 accumulation. A23187, bradykinin, and thrombin stimulated prostacyclin release to approximately four, four, and two times the basal levels, respectively, whereas carbachol and NE had little effect upon prostacyclin release. These results suggest that the activation of phospholipase C and of phospholipase A2 in MCEC are regulated separately.
在小鼠脑内皮细胞（MCEC）中研究了受体激动剂介导的磷酸肌醇水解和前列环素的产生。在所检测的11种神经递质和神经调质中，在存在LiCl（20 mM）的情况下，卡巴胆碱、去甲肾上腺素（NE）、缓激肽和凝血酶显著增加了3H-肌醇磷酸的积累。[3H]肌醇单磷酸（[3H]IP1）的最大刺激分别达到卡巴胆碱、NE、缓激肽和凝血酶基础水平的约11倍、11倍、7倍和4倍。卡巴胆碱和NE的IP1积累的EC50值分别为34和0.16 microM。毒蕈碱拮抗剂阿托品和哌仑西平分别以0.3和30 nM的Ki值阻断了卡巴胆碱诱导的IP1积累。肾上腺素能拮抗剂哌唑嗪以0.1 nM的Ki值阻断了NE诱导的IP1积累。钙离子载体A23187、组胺、谷氨酸、加压素、血清素、血小板活化因子和P物质未刺激IP1积累。A23187、缓激肽和凝血酶分别刺激前列环素释放至基础水平的约4倍、4倍和2倍，而卡巴胆碱和NE对前列环素释放几乎没有影响。这些结果表明，MCEC中磷脂酶C和磷脂酶A2的激活是分别调节的。
