Amer M S, Doba N, Reis D J
Proc Natl Acad Sci U S A. 1975 Jun;72(6):2135-9. doi: 10.1073/pnas.72.6.2135.
Changes in cyclic nucleotide metabolism similar to those characteristic of the chronic forms of hypertension were observed in an acute neurogenic form of hypertension in rats produced by electrolytic lesions of the nucleus tractus solitarii. These changes that were evident 2 hr after the lesions were made included decreased cyclic AMP levels in the heart, increased cGMP:cAMP ratio, cAMP phosphodiesterase (3':5'-cAMP 5'-nucleotidohydrolase, EC 3.1.4.17) and guanylyl cyclase (GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2) activities in the aorta and decreased snesitivity of adenylyl cyclase (ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1) in both the aorta and heart to stimulation by the beta-adrenergic stimulant isoproterenol. These changes appear to depend on catecholamine release and are not due to mechanical distortion secondary to the increased arterial pressure. These studies provide biochemical support to the concept that the sympathetic nervous system may play a critical role in the initiation of the hypertensive syndrome and that chronic hypertension could result from the fixation of the biochemical effects of increased sympathetic activity.
在通过孤束核电解损伤产生的急性神经源性高血压大鼠中，观察到与慢性高血压形式特征相似的环核苷酸代谢变化。损伤后2小时明显出现的这些变化包括心脏中环磷酸腺苷（cAMP）水平降低、主动脉中鸟苷酸环化酶（cGMP）与cAMP的比率升高、cAMP磷酸二酯酶（3':5'-cAMP 5'-核苷酸水解酶，EC 3.1.4.17）和鸟苷酸环化酶（GTP焦磷酸裂解酶（环化），EC 4.6.1.2）活性增加，以及主动脉和心脏中腺苷酸环化酶（ATP焦磷酸裂解酶（环化），EC 4.6.1.1）对β-肾上腺素能兴奋剂异丙肾上腺素刺激的敏感性降低。这些变化似乎依赖于儿茶酚胺释放，而不是由于动脉压升高继发的机械扭曲。这些研究为交感神经系统可能在高血压综合征的引发中起关键作用以及慢性高血压可能源于交感神经活动增加的生化效应的固定这一概念提供了生化支持。
