BIOCHEMICAL CHANGES IN HEARTS OF HYPERTENSIVE RATS FOLLOWING DIETARY PROTEINS

分离出cAMP依赖的蛋白激酶同工酶(I型和II型 从10个月龄小鼠心脏组织的可溶性部分中 自发性高血压大鼠(SHR) 四种试验性饮食中的一种：低蛋白质(LP)(19%蛋白质)， 标准(STD)(24%蛋白质)、高蛋白(HP)(32%蛋白质)或高蛋白质 DEAE-纤维素层析法测定蛋氨酸(1.9%蛋氨酸)(MET)。这个 测定这些同工酶的活性和/或水平，以检查 饮食对酶促心脏磷酸化作用的影响 调节蛋白。在cAMP存在的情况下，I型的活动 与低脂饮食组相比，低脂饮食组的蛋白激酶降低了3倍和4倍 32%组和蛋氨酸饲料组分别为SHR。II型蛋白 来自所有四个饮食组的激酶在小鼠体内表现出相似的活性 有没有露营。而心脏中的cAMP结合活性 STD、HP和MET组大鼠的组份与蛋白激酶相关 脂蛋白心脏部分的活性、cAMP结合活性 对照组大鼠的酶活性均高于对照组。在 磷蛋白(肌浆网(SR)蛋白，其磷酸化 [Ca~(2+)-Mg~(2+)]-ATPase磷酸化对钙转运的调节 研究表明，cAMP的加入显著刺激了磷蛋白 所有饮食组的磷酸化，但刺激的程度是 在MET组动物中最高，在LP组中最低 意义重大。发现的I型同工酶活性的降低 进食低蛋白饮食的自发性高血压大鼠的心脏部分可能是由于 酶对cAMP的反应或酶数量的减少 分子。这种情况可能会影响蛋白的磷酸化程度。 心脏调节蛋白，从而损害心脏生理 高血压。

cAMP-dependent protein kinase isozymes (Type I and Type II) were isolated from the soluble fractions of cardiac tissue from 10-month-old spontaneously hypertensive rats (SHR) which had been maintained for nine months on one of four experimental diets: low protein (LP) (19% protein), standard (STD) (24% protein), high protein (HP) (32% protein) or high methionine (1.9% methionine) (MET) by DEAE-cellulose chromatography. The activity and/or levels of these isozymes were determined to examine the influence of diet on the enzyme's effect on the phosphorylation of cardiac regulatory proteins. In the presence of cAMP the activity of the Type I protein kinase was reduced by 3 and 4-fold in the LP diet group compared to the SHR on 32% and methionine diet groups respectively. Type II protein kinase from all four diet groups exhibited similar activities in the presence and absence of cAMP. While cAMP-binding activities in the cardiac fractions from STD, HP and MET groups of rats correlate to protein kinase activities, cAMP-binding activities in the cardiac fractions from the LP group of rats by contrast were higher than enzyme activities. In the phospholamban (sarcoplasmic reticulum (SR) protein whose phosphorylation regulates CA2+ transport mediated by [Ca2+-Mg2+]-ATPase) phosphorylation study, addition of cAMP significantly stimulated phospholamban phosphorylation in all diet groups but the extent of stimulation was highest in the MET group of animals and lowest in the LP groups was not significant. The decrease in the activity of Type I isozyme found in the cardiac fractions from SHR fed low protein diet may be due to a defect in response of the enzyme to cAMP or a reduction in the number of enzyme molecules. Such a condition may affect the degree of phosphorylation of cardiac regulatory proteins, thus impairing cardiac physiology in hypertension.