Comprehensive Physiology 2019
DOI: 10.1002/cphy.c180039
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Redox Regulation of the Microcirculation

Abstract: The microcirculation maintains tissue homeostasis through local regulation of blood flow and oxygen delivery. Perturbations in microvascular function are characteristic of several diseases and may be early indicators of pathological changes in the cardiovascular system and in parenchymal tissue function. These changes are often mediated by various reactive oxygen species and linked to disruptions in pathways such as vasodilation or angiogenesis. This overview compiles recent advances relating to redox regulati… Show more

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Cited by 8 publications
(5 citation statements)
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“…The erythrocyte is considered to control the local blood flow via three possible nitric oxide‐mediated mechanisms: (i) release ATP to stimulate the production of nitric oxide by the endothelial cells, (ii) release nitric oxide derived from nitrosohaemoglobin, and (iii) release nitric oxide derived from the nitric oxide synthases and the nitrate–nitrite–nitric oxide reduction pathway in the erythrocyte 104,176,454,508–518 . Products of normal nitrogen metabolism, such as nitrosothiols 100 and peroxynitrite, can also induce vasodilation 519–522 . During low oxygen tension, the erythrocyte deformation increases ATP release via the activation of mechanosensitive Piezo1 channels 523 .…”
Section: The Dynamics Of Erythrocyte Metabolismmentioning
confidence: 99%
See 1 more Smart Citation
“…The erythrocyte is considered to control the local blood flow via three possible nitric oxide‐mediated mechanisms: (i) release ATP to stimulate the production of nitric oxide by the endothelial cells, (ii) release nitric oxide derived from nitrosohaemoglobin, and (iii) release nitric oxide derived from the nitric oxide synthases and the nitrate–nitrite–nitric oxide reduction pathway in the erythrocyte 104,176,454,508–518 . Products of normal nitrogen metabolism, such as nitrosothiols 100 and peroxynitrite, can also induce vasodilation 519–522 . During low oxygen tension, the erythrocyte deformation increases ATP release via the activation of mechanosensitive Piezo1 channels 523 .…”
Section: The Dynamics Of Erythrocyte Metabolismmentioning
confidence: 99%
“…104,176,454,[508][509][510][511][512][513][514][515][516][517][518] Products of normal nitrogen metabolism, such as nitrosothiols 100 and peroxynitrite, can also induce vasodilation. [519][520][521][522] During low oxygen tension, the erythrocyte deformation increases ATP release via the activation of mechanosensitive Piezo1 channels. 523 On the other, limited ATP release has been shown to impair microvascular blood flow.…”
Section: The Erythrocyte Transports Carbon Dioxide and Buffers Ph In ...mentioning
confidence: 99%
“…IN HYPERGLYCEMIA Sources of ROS in endothelial cells are NADPH oxidases, mitochondrial respiratory chain, NOS, xanthine oxidases, peroxidases, cyclooxygenases, and lipoxygenases [194][195][196]. NADPH oxidase which catalyzes the production of superoxide anion radical, a precursor of other ROS, is a main player.…”
Section: The Role Of Reactive Oxygen Species In Vascular Dysfunctionmentioning
confidence: 99%
“…Значимое снижение вклада Аэ частотного спектра регуляции МКЦ, наблюдаемое у больных с ХСН, по сравнению с группой контроля (4,9 vs 12,3%) (рисунок 2), можно рассматривать как проявление выраженной эндотелиальной дисфункции. Отсутствие корреляций между Аэ и параметрами внутрисердечной гемодинамики представляется весьма логичным в связи с большей зависимостью этого регуляторного компонента частотного спектра от локальных нейрогормональных механизмов [8,17,[21][22][23][24]. Хорошо известна роль оксида азота, простациклина, некоторых интерлейкинов, кальцитонин-ген-родственного пептида, субстанции Р во влиянии на тонус сосудов микроциркуляторного русла [2,16,25], однако оценка влияния многих других биологически активных молекул (гаптоглобина, копептина и др.)…”
Section: таблицаunclassified
“…Принято считать, что спазмирование артериол и прекапилляров, а также извилистость и полнокровие посткапилляров и собирательных венул, выявляемые при морфологических исследованиях у больных с ХСН [19,20], носят приспособительный характер и направлены на улучшение транскапиллярного обмена путем увеличения перфузионного давления [21][22][23]. Таким образом, выявленные в настоящем исследовании корреляционные взаимосвязи между Ам и ФВ ЛЖ, систолическими и диастолическими размерами и объемами ЛЖ (таблица 5) свидетельствуют о компенсаторном повышении мышечного тонуса прекапилляров при прогрессировании ХСН.…”
Section: заключениеunclassified