[Cyclic AMP in the kidneys of adrenalectomized and nonadrenalectomized normal rats and rats with reflex dystrophy against a background of organ denervation and a total block of the body's beta-adrenoreceptors by propranolol].

Ia I Azhipa, L K Egorova
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Abstract

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.

[肾上腺切除和非肾上腺切除的正常大鼠和反射性营养不良大鼠在器官去神经支配和心得安完全阻断身体β -肾上腺素受体的背景下肾脏中的环AMP]。
用放射免疫法研究了慢性坐骨神经刺激引起的反射性营养不良大鼠肾cAMP的含量,这些大鼠是由器官去神经支配或普萘洛尔阻断-肾上腺素引起的。结果表明,在正常情况下,尤其是在反射性营养不良的情况下,肾脏手术去神经支配导致肾cAMP升高。在坐骨神经完整的动物中,用心得安阻断β -肾上腺素能受体可伴有肾核苷酸的减少。基于自身和文献资料,我们认为坐骨神经损伤的焦点在病理刺激下对反射性营养不良的肾醛固酮受体的损害,以及它们在手术或药物(β -肾上腺素能受体阻断)失交感中功能的改善,可能是cAMP含量的改变。通过camp依赖性蛋白激酶,该核苷酸触发细胞内代谢转化的复杂系统,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的生化系统,参与了肾小管细胞发生反射性营养不良的损伤和正常化过程。
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