Journal of hypertension · 2020
Chronic exercise mediates epigenetic suppression of L-type Ca2+ channel and BKCa channel in mesenteric arteries of hypertensive rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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.
Zhang Yanyan, Chen Yu, Xu Zhaoxia, Wu Ying, Zhang Yimin, Shi Lijun
Аннотация
BACKGROUND: Regular exercise is a lifestyle intervention for controlling hypertension and has an improving effect on vascular function. Voltage-gated L-type Ca (LTCC) and large-conductance Ca-activated K (BKCa) channels are two principal mediators of vascular smooth muscle cell contractility and arterial tone. The present study tested the hypothesis that DNA methylation dynamics plays a key role in exercise-induced reprogramming and downregulation of LTCC and BKCa channel in mesenteric arteries from spontaneously hypertensive rats (SHRs).
METHODS: SHRs and Wistar-Kyoto (WKY) rats were subjected to exercise training or kept sedentary, and vascular molecular and functional properties were evaluated.
RESULTS: Exercise inhibited hypertension-induced upregulation of LTCC and BKCa channel function in mesenteric arteries by repressing LTCC α1c and BKCa β1 subunit expression. In accordance, exercise triggered hypermethylation of α1c and β1 gene in SHR, with concomitant decreasing TET1, increasing DNMT1 and DNMT3b expression in mesenteric arteries, as well as altering peripheral α-KG and S-adenosylmethionine/ S-adenosylhomocysteine ratio. Acting synergistically, these exercise-induced functional and molecular amelioration could allow for attenuating hypertension-induced elevation in arterial blood pressure.
CONCLUSION: Our results indicate that exercise suppresses LTCC and BKCa channel function via hypermethylation of α1c and β1 subunits, which contributes to the restoration of mesenteric arterial function and vasodilation during hypertension.
METHODS: SHRs and Wistar-Kyoto (WKY) rats were subjected to exercise training or kept sedentary, and vascular molecular and functional properties were evaluated.
RESULTS: Exercise inhibited hypertension-induced upregulation of LTCC and BKCa channel function in mesenteric arteries by repressing LTCC α1c and BKCa β1 subunit expression. In accordance, exercise triggered hypermethylation of α1c and β1 gene in SHR, with concomitant decreasing TET1, increasing DNMT1 and DNMT3b expression in mesenteric arteries, as well as altering peripheral α-KG and S-adenosylmethionine/ S-adenosylhomocysteine ratio. Acting synergistically, these exercise-induced functional and molecular amelioration could allow for attenuating hypertension-induced elevation in arterial blood pressure.
CONCLUSION: Our results indicate that exercise suppresses LTCC and BKCa channel function via hypermethylation of α1c and β1 subunits, which contributes to the restoration of mesenteric arterial function and vasodilation during hypertension.