Clinical Implications of Assessing Coronary Flow Velocity Reserve and Plasma Endothelin-1 in Hypertensive Patients

Fujii, Hideki; Takiuchi, Shin; Kamide, Kei; Horio, Takeshi; Niizuma, S.; Tanaka, Norio; Hashimoto, Shuji; Nakatani, Satoshi; Fukagawa, Masafumi; Kawano, Yuhei

doi:10.1291/hypres.28.911

Cited by 10 publications

(6 citation statements)

References 30 publications

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“…ET-1 levels in established hypertension and after acute myocardial infarction are in the range of 1 to 4.5 pg/mL, which is similar to that of our subjects. 54,55 In contrast, IL-6 levels in our healthy subjects were substantially lower than those seen in acute coronary syndromes, which can exceed 100 pg/mL. 56,57 The sICAM-1 levels in our subjects were lower than are levels typically seen in patients after stroke and acute coronary syndrome (244-340 ng/mL).…”

Section: Discussionmentioning

confidence: 53%

Inflammation and Sleep in Healthy Individuals

Mills

Känel

Norman

et al. 2007

Sleep

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Section: Discussionmentioning

confidence: 53%

Inflammation and Sleep in Healthy Individuals

Mills

Känel

Norman

et al. 2007

Sleep

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“…However, systemic acute infusion of ET-1 to raise its plasma level by 3–12 fold causes inhibition of cardiac function but does not elicit ischemia in human hearts [72–74]. It is worth noting that the ET-1 in patients with coronary diseases is only increased 2–4 fold [10–12, 14], which is unlikely to elicit significant vasoconstriction and consequently compromise coronary perfusion. Interestingly, the arterial and coronary sinus ET-1 levels did not change significantly in the patients who manifest close association between higher resting ET-1 level and the severity of reduced myocardial perfusion [75].…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 impairs coronary arteriolar dilation: Role of p38 kinase-mediated superoxide production from NADPH oxidase

Thengchaisri

Hein

Ren

et al. 2015

Journal of Molecular and Cellular Cardiology

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Elevated levels of endothelin-1 (ET-1), a potent vasoactive peptide, are implicated as a risk factor for cardiovascular diseases by exerting vasoconstriction. The aim of this study was to address whether ET-1, at sub-vasomotor concentrations, elicits adverse effects on coronary microvascular function. Porcine coronary arterioles (50–100 μm) were isolated, cannulated and pressurized without flow for in vitro study. Diameter changes were recorded using a videomicrometer. Arterioles developed basal tone (60±3 μm) and dilated to the endothelium-dependent nitric oxide (NO)-mediated vasodilators serotonin (1 nmol/L to 0.1 μmol/L) and adenosine (1 nmol/L to 10 μmol/L). Treating the vessels with a clinically relevant sub-vasomotor concentration of ET-1 (10 pmol/L, 60 minutes) significantly attenuated arteriolar dilations to adenosine and serotonin but not to endothelium-independent vasodilator sodium nitroprusside. The arteriolar wall contains ETA receptors and the adverse effect of ET-1 was prevented by ETA receptor antagonist BQ123, the superoxide scavenger Tempol, the NADPH oxidase inhibitors apocynin and VAS2870, the NOX2-based NADPH oxidase inhibitor gp91 ds-tat, or the p38 kinase inhibitor SB203580. However, ETB receptor antagonist BQ788, H2O2 scavenger catalase, scrambled gp91 ds-tat, or inhibitors of xanthine oxidase (allopurinol), PKC (Gö 6983), Rho kinase (Y27632), and c-Jun N-terminal kinase (SP600125) did not protect the vessel. Immunohistochemical staining showed that ET-1 elicited Tempol-, apocynin- and SB203580-sensitive superoxide production in the arteriolar wall. Our results indicate that exposure of coronary arterioles to a pathophysiological, sub-vasomotor concentration of ET-1 leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 kinase-mediated production of superoxide from NADPH oxidase following ETA receptor activation.

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“…ET A receptors are coupled to G‐protein (G q ) signaling, phospholipase activation, and Ca 2+ channels (similar to AT 1 and α 1 receptor signaling) [ 6 , 128 , 222 ]. ET‐1 is recognized as a mediator of endothelial dysfunction in coronary artery disease, as elevated plasma ET‐1 concentration is associated with decreased coronary blood flow reserve in humans [ 71 ].…”

Section: Coronary Endothelial Function In Obesity and Insulin Resistancementioning

confidence: 99%

Mechanisms of Coronary Dysfunction in Obesity and Insulin Resistance

et al. 2007

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The incidence of obesity and the metabolic syndrome has reached epidemic proportions and alterations in coronary microvascular function could contribute to the increased cardiovascular morbidity and mortality observed in these patients. This review highlights key mechanisms of impaired control of coronary blood flow in the metabolic syndrome. Specifically, coronary endothelial dysfunction, altered neurohumoral control, and the potential roles of smooth muscle ion channels are addressed. Recent studies indicate that alterations in endothelial-dependent vasodilation or endothelial-dependent vasoconstriction contribute little to obesity-induced impairments in coronary vascular control. In contrast, augmented vasoconstriction in response to neurohumoral mediators appears to play a significant role in coronary vascular dysfunction. The authors conclude that coronary dysfunction in the metabolic syndrome is characterized by an imbalance between coronary blood flow and myocardial metabolism that may be mediated by sensitization of vasoconstrictor pathways. Further, they suggest that alterations in smooth muscle ion channels, Ca(2+) handling, and cell signaling may be important mechanisms leading to coronary microvascular dysfunction. Importantly, however, more research is needed to clearly delineate specific mechanisms and identify potential therapeutic targets.

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Clinical Implications of Assessing Coronary Flow Velocity Reserve and Plasma Endothelin-1 in Hypertensive Patients

Cited by 10 publications

References 30 publications

Inflammation and Sleep in Healthy Individuals

Inflammation and Sleep in Healthy Individuals

Endothelin-1 impairs coronary arteriolar dilation: Role of p38 kinase-mediated superoxide production from NADPH oxidase

Mechanisms of Coronary Dysfunction in Obesity and Insulin Resistance

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