Okayama H, Hamada M, Kawakami H, Ikeda S, Hashida H, Shigematsu Y, Hiwada K
Second Department of Internal Medicine, Ehime University School of Medicine, Japan.
J Hypertens. 1997 Dec;15(12 Pt 2):1767-74. doi: 10.1097/00004872-199715120-00087.
To clarify whether the functional changes during the transition from compensatory myocardial hypertrophy to failure are associated with changes in sarcoplasmic reticulum gene expression.
We examined the gene expression of sarcoplasmic reticulum proteins [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, calsequestrin and ryanodine receptor] in Dahl salt-sensitive (Dahl-S) rats fed a high-salt (8%) diet from the age of 6 weeks. In-vivo contractile functioning was evaluated using echocardiography, and gene expression of sarcoplasmic reticulum proteins in the left ventricle was analyzed by Northern blotting for each stage of left ventricular hypertrophy.
SERCA messenger RNA (mRNA) levels in Dahl-S rats with compensatory hypertrophy did not change significantly, whereas phospholamban mRNA levels were increased by 61% (P < 0.01), and calsequestrin mRNA levels were increased by 130% (P < 0.01) compared with those in Dahl salt-resistant (Dahl-R) rats. SERCA mRNA levels in Dahl-S rats with decompensated dilatation were decreased by 32% (P< 0.05), whereas levels of phospholamban and calsequestrin mRNA remained unchanged. Ryanodine receptor mRNA levels did not change either with compensatory hypertrophy or with decompensated dilatation.
Alterations in expression of sarcoplasmic reticulum gene may be related to changes in systolic and diastolic properties in compensatory hypertrophy and heart failure.
明确从代偿性心肌肥大转变为心力衰竭过程中的功能变化是否与肌浆网基因表达的改变相关。
我们检测了6周龄起喂食高盐(8%)饮食的 Dahl 盐敏感(Dahl-S)大鼠肌浆网蛋白[肌浆网 Ca2+ -ATP 酶(SERCA)、受磷蛋白、肌集钙蛋白和雷诺丁受体]的基因表达。使用超声心动图评估体内收缩功能,并通过 Northern 印迹法分析左心室肥厚各阶段左心室肌浆网蛋白的基因表达。
代偿性肥大的 Dahl-S 大鼠中 SERCA 信使核糖核酸(mRNA)水平无显著变化,而与 Dahl 盐抵抗(Dahl-R)大鼠相比,受磷蛋白 mRNA 水平增加了61%(P < 0.01),肌集钙蛋白 mRNA 水平增加了130%(P < 0.01)。失代偿性扩张的 Dahl-S 大鼠中 SERCA mRNA 水平降低了32%(P < 0.05),而受磷蛋白和肌集钙蛋白 mRNA 水平保持不变。雷诺丁受体 mRNA 水平在代偿性肥大或失代偿性扩张时均未改变。
肌浆网基因表达的改变可能与代偿性肥大和心力衰竭时的收缩和舒张特性变化有关。