PI-response and Signal Tranadut in Myocardial Gamage

在许多不同荷尔蒙和神经发射器的作用机制中，主要事件发生在离子体膜蛋白质肌醇磷脂的破坏中，受试者介导的刺激。这种称为磷酸磷酰肌醇（PI）的转弯路径产生两个第二次信使，肌醇-（1， 4，5）三磷酸盐（IP_3）和sn 1，2-二乙酰甘油醇（DAG）。DAG刺激膜绑定磷酸脂依赖， Ca^<2+>-依赖蛋白激酶C，同时IP_3释放Ca^<2+>从内塑性视网膜存储。我们认为，Pl--转弯路径在诱导心脏病myocyte hypertrophy中有一个非常重要的作用。这个实验的目的是研究高毒性大鼠心脏中的肌醇三磷酸激酶的性质。在目前的实验中，我们演示了肌醇-（1， 4， 5）三磷酸盐（IP_3）激酶活动在自发的高毒性大鼠（SHRSP）心脏中被添加到Wistar Kyoto大鼠（WKY）。IP_3激酶在心脏中的活性在SHRSP和WKY中都是最高的。它在SHRSP年龄5至20周内不断增加的活动。该活动在5周旧的SHRSP中达到了3次，达到了40周旧的SHRSP水平。在另一只手里，它是1.3-折叠在40周，与5周旧相比。我们确定了IP_3激酶活动中的差异效应。Ca^<2+>刺激其活动在10^<-9>到10 ^<-6>M。在SHRSP中，它增强了大约2.1-折叠在10^<-6>M的Ca^<2+>，但在WKY中，折叠在10^<-6>M的Ca^<2+>。Mn^<2+>也刺激了IP_3激酶活动，同时， Fe^<2+>， Zn^<2 +>和Cu^<2+>抑制了IP_3激酶活动。在我们的实验中，IP_3激酶活动在SHRSP中增加，其活动在市场上受到分歧的影响。These data suggest the accumulations of IP_3 and IP_4 after hormonal stimulation have a physiologic role， possibly by alteration of Ca^<2+> levels in cardiac tissue。

The primary event in the mechanism of action of many different hormones and neurotransmitters involves receptor-mediated stimulation of the breakdown of plasma membrane inositol phospholipids. This so-called phosphatidylinositol (PI) turnover pathway generates two second messengers, inositol- (1, 4,5) trisphosphate (IP_3) and sn 1, 2-diacyglycerol (DAG). DAG stimulates membrane-bound phospho-lipid-dependent, Ca^<2+>-dependent protein kinase C while IP_3, releases Ca^<2+> from endoplasmic reticulum stores. We consider that Plーturnover pathway has a quite important role in inducing cardiac myocyte hypertrophy. The purpose of this experiment is to study the properties of inositoltrisphostate kinase in hypertrophied rat heart.In the present experiment, we demonstrated that inositol- (1, 4, 5) tris-phosphate (IP_3) kinase activity was increased in the stroke-prone spontaneously hypertensive rat (SHRSP) heart compared to the Wistar Kyoto rat (WKY). IP_3 kinase activity in the heart was highest in the cytosolic fraction in both SHRSP and WKY. Its activity progressively increased with age in SHRSP aged 5 to 20 weeks. The activity reached about three times the level of 5-week-old SHRSP in 40-weeks-old SHRSP. On the other hand, in WKY it was 1.3-fold at 40 weeks compared with 5-week-olds. We determined the effect of divalent cations on IP_3 kinase activity. Ca^<2+> stimulated its activity in a dose-dependent manner at 10^<-9> to 10^<-6>M. In SHRSP it was enhanced about 2.1-fold at 10^<-6>M of Ca^<2+>, but in WKY it was 1.5-fold at 10^<-6>M of Ca^<2+>. Mn^<2+> also stimulated IP_3 kinase activity in both groups of animals, while, Fe^<2+>, Zn^<2+>, and Cu^<2+> inhibited IP_3 kinase activity. In our experiment IP_3 kinase activity was increased in SHRSP and its activity was markedly affected by divalent cations. These data suggest the accumulations of IP_3 and IP_4 after hormonal stimulation have a physiologic role, possibly by alteration of Ca^<2+> levels in cardiac tissue.