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Akimov, Yu. A.; Kositsyn, N. S.

doi:10.1023/a:1020417927424

Biology Bulletin of the Russian Academy of Sciences

2002

DOI: 10.1023/a:1020417927424

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Yu. A. Akimov

N. S. Kositsyn

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Cited by 3 publications

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“…In particular, inadequate neurotrophic support proved to change its functional status (Azhipa and Filyashina, 1963). It was shown that the kidney suffering from NDP had a different sensitivity to physiologically active substances including hormones (Azhipa, 1974) and mineralocorticoid aldosterone, in particular (Azhipa and Filyashina, 1980;Akimov andKositsin, 2002, 2003). It was manifested as defective reabsorption of sodium ion during NDP and inadequate renal response to aldosterone administration, which normally increases reabsorption of this ion (Crabbe, 1966(Crabbe, , 1972 due to the effect of aldosterone on sodium transport in cells of many tissues and organs, particularly, in cells of renal tubules (Losert et al ., 1964;Marver et al ., 1974).…”

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Mechanisms of neurogenic dystrophies induced by activation and deprivation of the sympathetic nervous system

Akimov

Kositsyn

2005

Biol Bull Russ Acad Sci

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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. β -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. ANIMAL PHYSIOLOGY

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confidence: 99%

Mechanisms of neurogenic dystrophies induced by activation and deprivation of the sympathetic nervous system

Akimov

Kositsyn

2005

Biol Bull Russ Acad Sci

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RAAS escape: A real clinical entity that may be important in the progression of cardiovascular and renal disease

Lakkis¹,

Lü²,

Weir

2003

Current Science Inc

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Interruption of the renin-angiotensin-aldosterone system (RAAS) at different levels is target-organ protective in several disease states; however, complete blockade is unlikely to be achieved due to escape mechanisms whenever blockade is attempted, incomplete knowledge of the role of all elements of the RAAS, and lack of pharmacotherapy against some elements that have been shown to contribute to disease states. Aldosterone has been overlooked as a mediator of RAAS escape and a key factor in target-organ injury despite the use of available RAAS blockers. Aldosterone is thought to play a role in the development of hypertension, alteration in vascular structure, vascular smooth muscle hypertrophy, endothelial dysfunction, structural renal injury, proteinuria, left ventricular remodeling, collagen synthesis, and myocardial fibrosis. Aldosterone receptor antagonists have been shown to antagonize all these effects in experimental models. Clinical trials with aldosterone antagonists showed an improvement in survival and left ventricular mass index in patients with congestive heart failure, and a reduction in urinary protein excretion and left ventricular mass index in patients with type 2 diabetes and early nephropathy who developed aldosterone synthesis escape. Consequently, aldosterone receptor antagonists may have specific benefits for reducing target-organ injury, particularly if there is evidence of RAAS escape.

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Effect of β Adrenoreceptor Blocker Propranolol during Reflex Renal Dystrophy Induced by Sciatic Nerve Cutting

Akimov

Kositsyn

2004

Biology Bulletin

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Cited by 3 publications

References 5 publications

Mechanisms of neurogenic dystrophies induced by activation and deprivation of the sympathetic nervous system

Mechanisms of neurogenic dystrophies induced by activation and deprivation of the sympathetic nervous system

RAAS escape: A real clinical entity that may be important in the progression of cardiovascular and renal disease

Effect of β Adrenoreceptor Blocker Propranolol during Reflex Renal Dystrophy Induced by Sciatic Nerve Cutting

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