对成年大鼠左心房中磷脂酰肌醇周转的刺激并不涉及肌醇（1,4,5）三磷酸的释放。

Stimulation of phosphatidylinositol turnover in adult rat left atria does not involve release of inositol(1,4,5)trisphosphate.

Anderson K E, Myers D, Woodcock E A

Cellular Biochemistry Laboratory, Baker Medical Research Institute, Prahran, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1993 May;20(5):335-8. doi: 10.1111/j.1440-1681.1993.tb01698.x.

Abstract

The turnover rate of inositol(1,4,5)trisphosphate (Ins(1,4,5)P3) in noradrenaline-stimulated adult rat left atria was calculated from changes in specific activity and was found to equal 110 ct/min per mg tissue. In contrast, the isomers of inositol mono- and bisphosphates accumulated at a rate of 508 ct/min per mg. 2. Neomycin, which inhibits release of Ins(1,4,5)P3, inhibited the accumulation of inositol phosphates in noradrenaline-stimulated isolated neonatal cardiomyocytes but did not inhibit accumulation in left atria. 3. These data demonstrate that most of the inositol phosphates which accumulate in adult rat left atria do not derive from Ins(1,4,5)P3. 4. These data are best explained by a model in which noradrenaline stimulation results mainly in the breakdown of phosphatidylinositol(4)monophosphate (PtIns(4)P1) to inositol(1,4)bisphosphate (Ins(1,4)P2). Thus, heart tissue avoids the generation of Ins(1,4,5)P3.

摘要

从比活性变化计算去甲肾上腺素刺激的成年大鼠左心房中肌醇（1,4,5）三磷酸（Ins(1,4,5)P3）的周转率，发现其等于每毫克组织110 ct/min。相比之下，肌醇单磷酸酯和双磷酸酯异构体的积累速率为每毫克508 ct/min。2. 抑制Ins(1,4,5)P3释放的新霉素抑制了去甲肾上腺素刺激的离体新生心肌细胞中肌醇磷酸酯的积累，但不抑制左心房中的积累。3. 这些数据表明，成年大鼠左心房中积累的大多数肌醇磷酸酯并非来自Ins(1,4,5)P3。4. 这些数据最好用一种模型来解释，即去甲肾上腺素刺激主要导致磷脂酰肌醇（4）单磷酸（PtIns(4)P1）分解为肌醇（1,4）双磷酸（Ins(1,4)P2）。因此，心脏组织避免了Ins(1,4,5)P3的产生。