Watson P A, Haneda T, Morgan H E
Sigfried and Janet Weis Center for Research, Geisinger Clinic, Danville, Pennsylvania 17822.
Am J Physiol. 1989 Jun;256(6 Pt 1):C1257-61. doi: 10.1152/ajpcell.1989.256.6.C1257.
Elevation of aortic perfusion pressure from 60 to 120 mmHg in beating and arrested rat hearts raised cAMP content and increased rates of ribosome formation but had no effect on total protein synthesis during 1 h of perfusion. The activity of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase increased as perfusion pressure was elevated in arrested hearts. A regulatory link between increased cAMP content and accelerated ribosome formation was hypothesized to exist. When hearts were arrested with tetrodotoxin and exposed to 0.2 mM methacholine, a muscarinic-cholinergic agonist that blocked pressure-induced increases in cAMP content, elevation of aortic pressure to 120 mmHg failed to increase the rate of ribosome formation. When aortic pressure was maintained at 60 mmHg, exposure of beating hearts to glucagon increased cAMP content and mimicked the effect of elevated aortic pressure to accelerate rates of ribosome formation. These studies support the hypothesis that increased aortic pressure preferentially accelerates rates of ribosome formation by a cAMP-dependent mechanism.
在跳动和停搏的大鼠心脏中，将主动脉灌注压从60 mmHg提高到120 mmHg，可使环磷酸腺苷（cAMP）含量升高，核糖体形成速率增加，但在1小时的灌注过程中对总蛋白合成没有影响。在停搏的心脏中，随着灌注压升高，3',5'-环磷酸腺苷（cAMP）依赖性蛋白激酶的活性增加。据推测，cAMP含量增加与核糖体形成加速之间存在调节联系。当心脏用河豚毒素停搏并暴露于0.2 mM乙酰甲胆碱（一种能阻断压力诱导的cAMP含量增加的毒蕈碱型胆碱能激动剂）时，将主动脉压力升高到120 mmHg未能增加核糖体形成速率。当主动脉压力维持在60 mmHg时，将跳动的心脏暴露于胰高血糖素会增加cAMP含量，并模拟主动脉压力升高对加速核糖体形成速率的影响。这些研究支持了以下假设：主动脉压力升高通过cAMP依赖性机制优先加速核糖体形成速率。
