Erythropoietin enhances hydrogen peroxide-mediated dilatation of canine coronary collateral arterioles during myocardial ischemia in dogs in vivo

Yada, Toyotaka; Shimokawa, Hiroaki; Hiramatsu, Osamu; Satoh, Minoru; Kashihara, Naoki; Takaki, Akira; Goto, Masami; Ogasawara, Yasuo; Kajiya, Fumihiko

doi:10.1152/ajpheart.00331.2010

Cited by 7 publications

(8 citation statements)

References 51 publications

(66 reference statements)

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“…Coronary microcirculation plays an important role in maintaining blood flow and vascular homeostasis under both physiological and pathological conditions. We have confirmed that EDH plays an important compensatory role during coronary autoregulation and reperfusion injury in ischemic and collateral microcirculation in dogs in vivo through compensation of NO. Endothelial dysfunction has been implicated in the reduced dilatation of porcine coronary microcirculation .…”

Section: Introductionsupporting

confidence: 70%

Endothelium‐dependent hyperpolarization‐mediated vasodilatation compensates nitric oxide‐mediated endothelial dysfunction during ischemia in diabetes‐induced canine coronary collateral microcirculation in vivo

2018

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Section: Introductionsupporting

confidence: 70%

Endothelium‐dependent hyperpolarization‐mediated vasodilatation compensates nitric oxide‐mediated endothelial dysfunction during ischemia in diabetes‐induced canine coronary collateral microcirculation in vivo

2018

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“…Erythropoietin (EPO) reduces oxidative stress and facilitates NO production (and also that of H 2 O 2 ; see section ) and thus prevents endothelial dysfunction resulting from eNOS uncoupling both in vivo and in vitro (Yada et al . , Kuriyama et al . , d'Uscio et al .…”

Section: Nitric Oxidementioning

confidence: 99%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

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The endothelium can evoke relaxations of the underlying vascular smooth muscle, by releasing vasodilator substances. The best-characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which activates soluble guanylyl cyclase in the vascular smooth muscle cells, with the production of cyclic guanosine monophosphate (cGMP) initiating relaxation. The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDH-mediated responses). As regards the latter, hydrogen peroxide (H O ) now appears to play a dominant role. Endothelium-dependent relaxations involve both pertussis toxin-sensitive G (e.g. responses to α -adrenergic agonists, serotonin, and thrombin) and pertussis toxin-insensitive G (e.g. adenosine diphosphate and bradykinin) coupling proteins. New stimulators (e.g. insulin, adiponectin) of the release of EDRFs have emerged. In recent years, evidence has also accumulated, confirming that the release of NO by the endothelial cell can chronically be upregulated (e.g. by oestrogens, exercise and dietary factors) and downregulated (e.g. oxidative stress, smoking, pollution and oxidized low-density lipoproteins) and that it is reduced with ageing and in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and EDH, in particular those due to H O ), endothelial cells also can evoke contraction of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factors. Recent evidence confirms that most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells and that prostacyclin plays a key role in such responses. Endothelium-dependent contractions are exacerbated when the production of nitric oxide is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive and diabetic patients. In addition, recent data confirm that the release of endothelin-1 can contribute to endothelial dysfunction and that the peptide appears to be an important contributor to vascular dysfunction. Finally, it has become clear that nitric oxide itself, under certain conditions (e.g. hypoxia), can cause biased activation of soluble guanylyl cyclase leading to the production of cyclic inosine monophosphate (cIMP) rather than cGMP and hence causes contraction rather than relaxation of the underlying vascular smooth muscle.

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“…Tetraethylammonium-sensitive K + channels (BK Ca or K V ) in the coronary microvasculature are redox-sensitive targets in the cardioprotective effect of endogenous H 2 O 2 during ischemia-reperfusion injury (997). In the dog heart, erythropoietin enhances the H 2 O 2 - and BK Ca -mediated dilation of coronary collateral arterioles during ischemia (999). Redox-sensitive K V (but not BK Ca ) channels mediate H 2 O 2 -induced vasodilation in canine coronary arterioles and in the canine heart in vivo (799).…”

Section: Ion Channels As End Effectorsmentioning

confidence: 99%

Regulation of Coronary Blood Flow

Goodwill

Dick

Kiel

et al. 2017

Comprehensive Physiology

244

248

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The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery.

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Erythropoietin enhances hydrogen peroxide-mediated dilatation of canine coronary collateral arterioles during myocardial ischemia in dogs in vivo

Cited by 7 publications

References 51 publications

Endothelium‐dependent hyperpolarization‐mediated vasodilatation compensates nitric oxide‐mediated endothelial dysfunction during ischemia in diabetes‐induced canine coronary collateral microcirculation in vivo

Endothelium‐dependent hyperpolarization‐mediated vasodilatation compensates nitric oxide‐mediated endothelial dysfunction during ischemia in diabetes‐induced canine coronary collateral microcirculation in vivo

Endothelial dysfunction and vascular disease - a 30th anniversary update

Regulation of Coronary Blood Flow

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