Dimitrov D, Resink T J, Müller F B, Bühler F R
J Hypertens Suppl. 1986 Dec;4(6):S346-8.
The metabolism of phosphoinositides was investigated in platelet membranes from nine patients with essential hypertension (EHT) and from 10 age/sex-matched normotensive subjects. 32P-labelling or phosphatidic acid (PA), phosphatidylinositol (PI), phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2) was measured in lipid extracts prepared from resting 32P-prelabelled platelets. There were no differences in 32P-PA between subject groups. In platelets of hypertensive patients, 32P-incorporation into both PIP and PIP2 was greater (P at least less than 0.01). This increase apparently occurred at the expense of lower 32P-incorporation into PI (P less than 0.001). An alteration in the interconversion equilibrium between phosphoinositides which is directed towards polyphosphoinositide formation may lead to altered membrane ionic fluxes.
对9名原发性高血压（EHT）患者和10名年龄/性别匹配的血压正常受试者的血小板膜中磷酸肌醇的代谢情况进行了研究。在从预先用32P标记的静息血小板制备的脂质提取物中，测定了32P标记的磷脂酸（PA）、磷脂酰肌醇（PI）、磷脂酰肌醇-4-磷酸（PIP）和磷脂酰肌醇-4,5-二磷酸（PIP2）。受试者组之间的32P-PA没有差异。在高血压患者的血小板中，32P掺入PIP和PIP2的量均更多（P至少小于0.01）。这种增加显然是以较低的32P掺入PI为代价的（P小于0.001）。磷酸肌醇之间相互转化平衡朝着多磷酸肌醇形成方向的改变可能会导致膜离子通量的改变。
