Van Rooijen L A, Bazan N G
Biochem Biophys Res Commun. 1986 Jan 14;134(1):378-85. doi: 10.1016/0006-291x(86)90574-7.
Incubation of purified bovine photoreceptor rod outer segments with [gamma-32P]ATP resulted in the labeling of phosphatidylinositol 4-phosphate (PIP) and phosphatidic acid (PA) with little labeling of phosphatidylinositol 4,5-bisphosphate (PIP2). Propranolol inhibited in a dose-dependent manner the labeling of PA and enhanced that of PIP. Various cationic amphiphilic drugs also were tested for these effects. Propranolol had the same effects on high-speed rat brain particulate material. While this particular preparation displayed more labeling of PIP2, propranolol was ineffective, as it was on retinal PIP-kinase. Ca2+-activated polyphosphoinositide phosphodiesterase activity in nerve-ending membranes also was inhibited by propranolol. It is concluded that cationic amphiphilic drugs can inhibit diacylglycerol kinase and the polyphosphoinositide phosphodiesterase and stimulate the phosphatidylinositol-kinase (but not PIP-kinase).
用[γ-32P]ATP孵育纯化的牛感光细胞视杆外段，结果显示磷脂酰肌醇4-磷酸（PIP）和磷脂酸（PA）被标记，而磷脂酰肌醇4,5-二磷酸（PIP2）几乎没有被标记。普萘洛尔以剂量依赖性方式抑制PA的标记，并增强PIP的标记。还测试了各种阳离子两亲性药物的这些作用。普萘洛尔对高速离心的大鼠脑微粒体物质有相同的作用。虽然这种特定的制剂显示出更多的PIP2标记，但普萘洛尔无效，就像它对视网膜PIP激酶无效一样。神经末梢膜中Ca2+激活的多磷酸肌醇磷酸二酯酶活性也被普萘洛尔抑制。结论是阳离子两亲性药物可抑制二酰基甘油激酶和多磷酸肌醇磷酸二酯酶，并刺激磷脂酰肌醇激酶（但不刺激PIP激酶）。
