British journal of experimental pathology · 1979
Pathogenesis of the renal injury in choline deficiency: the role of catecholamines and acetylcholine.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Costa R S, Rossi M A, Oliveira J S
Аннотация
A disturbed renal circulation due to an imbalance between vasoconstrictor catecholamines and a vasodilator such as acetylcholine, caused by a decrease in acetylcholine, has been postulated as the basic mechanism of haemorrhagic degeneration of the kidneys in choline deficiency. To explore this hypothesis further a group of male weanling Wistar rats was fed on a choline-deficient diet for 10 days (Group CD). A control group was fed on the same basal diet supplemented with choline (Group CS). Food intake and body weights were registered. The kidneys of choline-supplemented and choline-deficient rats were studied grossly and histologically. The levels of catecholamines (noradrenaline and adrenaline) and acetylcholine were determined. Pathological changes of the kidneys were present in 30 out of 57 choline-deficient rats, permitting the separation of data obtained from deficient rats into those not associated with renal injury (CDa rats) and those associated with renal injury (CDb rats). A marked increase in the levels of renal catecholamines was observed in both CDa and CDb rats. On the other hand, the content of acetylcholine remained unchanged. It is noteworthy that the changes in tissue catecholamine levels occurred before there were changes in kidney weight and morphology. The findings support the concept that an imbalance between sympathetic and parasympathetic systems plays an important role in the pathogenesis of the renal injury of cholinedeficient weanling rats, and that this imbalance would be the result of an excess of catecholamines in the kidneys.