Информационная система "Конференции"

Abstracts

Receptors of distal renal channels were thought to be the only target of aldosteron action up to the recent time. It was also generally accepted that the main effect of aldosteron was sodium and water retention and the enhanced potassium excretion. Aldosteron is the most potential factor of inflammation and fibrosis, it enhances proteinuria due to the stimulation of the PAI-1 formation (plasminogen-1 activator inhibitor).

It was believed that ACE inhibitors and AT1 receptor antagonists decrease aldosteron formation by blocking the effects of angiotensin II. But there are other mechanisms of aldosteron stimulation. The increase of serum potassium concentration, induced by ACE inhibitors or AT1 receptor antagonists, stimulates the aldosteron formation. Thus the drugs mentioned above and which are widely used in case of cardiorenal pathology can stimulate the aldosteron formation mediated by the increase of potassium level. There are experimental data proving that the decrease of fibrosis in kidneys and the considerable antiproteinuric effect are provided by spironolactone or new selective angiotensin receptor antagonist - eplerenon. Now it is estimated that the aldosteron receptors are also located in brain, heart and vessels. We have evaluated the positive correlation between the plasma aldosteron level and the rate of the chronic renal failure progression.

Note. Abstracts are published in author's edition

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