[Mechanisms of neurogenic dystrophies induced by activation and deprivation of the sympathetic nervous system].
Entry of abnormal nervous stimuli after sciatic nerve transection proved to affect the functioning of renal mineralocorticoid receptors as a result of inadequate neurotrophic support of this organ. Drug blockade of both neural and humoral transmission of the abnormal stimuli from the injured nerve to the kidney prevented development of trophic disorders as indicated by the status of the renal mineralocorticoid receptor system. At the same time, drug stimulation of the sympathetic nervous system further affected aldosterone reception by this organ. beta-Blocker propranolol was shown to exert an antidystrophic effect in the case of local injuries of the neural system and, thus, prevented the development of neurogenic dystrophies.
Akimov
Iu A
IuA
Kositsyn
N S
NS
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D007668:Kidney / Q000294:innervation* / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology*; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D018161:Receptors, Mineralocorticoid / Q000502:physiology; D012584:Sciatic Nerve / Q000187:drug effects / Q000293:injuries; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000293:injuries / Q000503:physiopathology*
D000319:Adrenergic beta-Antagonists; D018161:Receptors, Mineralocorticoid; D007980:Levodopa; D000450:Aldosterone; D011433:Propranolol