Azhipa Ia I, Egorova L K
Izv Akad Nauk SSSR Biol. 1992 Sep-Oct(5):733-43.
Using the radioimmunological assay, renal cAMP content was studied in adrenalectomized and non-adrenalectomized rats with reflex dystrophy resulting from chronic ischiatic nerve stimulation against the background either of organ denervation or of general beta-adreno-blockade with propranolol. It was shown that the surgical denervation of kidney resulted in an increase in renal cAMP both in norm and especially in reflex dystrophy. The beta-adrenoceptor blockade with propranolol was accompanied by a decrease in renal nucleotide being more pronounced in animals with intact ischiatic nerve. Based on own and literature data we have suggested that one cause for the damage to renal aldosterone receptors in reflex dystrophy under pathological stimulation from the focus of damage in ischiatic nerve as well as for their improved functioning in surgical or pharmacological (beta-adrenoceptor blockade) desympathization which discontinues this stimulation, may be change in cAMP content. Via cAMP-dependent protein kinases, this nucleotide triggers a complex system of intracellular metabolic transformations which is able to change the protein spectrum of cytoplasm, nucleus, and chromatin and, therefore, the protein complex of aldosterone receptors. A participation of other biochemical systems of aldosterone stimulus transmission, including cAMP-independent ones, in processes of damage and normalization of tubule cells of the kidneys undergoing reflex dystrophy cannot be excluded.
利用放射免疫分析法,研究了去肾上腺和未去肾上腺大鼠在坐骨神经慢性刺激所致反射性营养不良状态下,在器官去神经支配或普萘洛尔全身β - 肾上腺素能阻滞背景下的肾环磷酸腺苷(cAMP)含量。结果表明,肾脏手术去神经支配在正常情况下,尤其是在反射性营养不良时,会导致肾cAMP增加。普萘洛尔对β - 肾上腺素能受体的阻滞伴随着肾核苷酸的减少,在坐骨神经完整的动物中更为明显。基于自身和文献数据,我们认为,在坐骨神经损伤灶的病理刺激下,反射性营养不良时肾醛固酮受体受损以及在手术或药理学(β - 肾上腺素能受体阻滞)去交感神经化(中断这种刺激)时其功能改善的一个原因,可能是cAMP含量的变化。通过依赖cAMP的蛋白激酶,这种核苷酸触发了一个复杂的细胞内代谢转化系统,该系统能够改变细胞质、细胞核和染色质的蛋白质谱,从而改变醛固酮受体的蛋白质复合物。不能排除醛固酮刺激传递的其他生化系统,包括不依赖cAMP的系统,参与了发生反射性营养不良的肾小管细胞损伤和恢复正常的过程。