Dobson J G
Am J Physiol. 1978 May;234(5):H638-45. doi: 10.1152/ajpheart.1978.234.5.H638.
The relationship between cAMP-dependent protein kinase activity and epinephrine-produced activation of phosphorylase and increase in contractility was investigated in the intact working rat heart. Epinephrine was administered as a bolus into the superior vena cava of open-chest preparations and the hearts were rapidly frozen. cAMP increased within 5 s and returned to control within 20-30 s. Protein kinase and phosphorylase kinase activity ratios increased transiently with the same time course as that for cAMP. The phosphorylase activity ratio and the rate of left ventricular pressure development increased maximally within 15 s and returned to control in 30-60 s. Continuous infusion of epinephrine caused a sustained elevation of the protein kinase. Free catalytic protein kinase activity increased proportionately with the dose of epinephrine. The beta-adrenergic blocking agent, practolol, had no effect on the basal levels of the five parameters studied, but did prevent the epinephrine-produced increases. The results suggest that the time course of cAMP-dependent protein kinase activation is appropriate if this enzyme is to play a role in the catecholamine-induced increase in both glycogenolysis and contractility in the in vivo heart.
在完整的工作大鼠心脏中，研究了环磷酸腺苷（cAMP）依赖性蛋白激酶活性与肾上腺素产生的磷酸化酶激活及收缩性增加之间的关系。将肾上腺素作为推注剂注入开胸制剂的上腔静脉，然后迅速冷冻心脏。cAMP在5秒内升高，并在20 - 30秒内恢复到对照水平。蛋白激酶和磷酸化酶激酶活性比与cAMP具有相同的时间进程而短暂升高。磷酸化酶活性比和左心室压力发展速率在15秒内最大程度升高，并在30 - 60秒内恢复到对照水平。持续输注肾上腺素导致蛋白激酶持续升高。游离催化蛋白激酶活性与肾上腺素剂量成比例增加。β - 肾上腺素能阻断剂心得宁对所研究的五个参数的基础水平没有影响，但确实阻止了肾上腺素引起的增加。结果表明，如果该酶要在体内心脏儿茶酚胺诱导的糖原分解和收缩性增加中发挥作用，cAMP依赖性蛋白激酶激活的时间进程是合适的。
