Increased Plasma Concentrations of Endothelin-1 and Big Endothelin-1 in Acute Myocardial Infarction

Miyauchi, Takashi; Yanagisawa, Masashi; Tomizawa, Takuji; Sugishita, Yasuro; Suzuki, Nobuhiro; Fujino, Masahiko; Ajisaka, Ryuichi; Goto, Katsutoshi; Masaki, Τοmoh

doi:10.1016/s0140-6736(89)90303-6

Cited by 544 publications

(199 citation statements)

References 8 publications

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“…It is well known that increased ET-1 levels are present in insulinresistant subjects, in Type 2 diabetic hyperlipidemic patients, and in atherosclerosis and cardiovascular disease (16,20,32). Moreover, in patients with coronary artery disease, a marked increase of ET-1 release was observed during exercise, in the presence of increased FFA levels (11).…”

Section: Effects Of Type 2 Diabetes Mellitus On Myocardial Insulin Rementioning

confidence: 99%

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Monti¹,

Landoni²,

Setola³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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dial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients. Am J Physiol Heart Circ Physiol 287: H1225-H1231, 2004. First published May 6, 2004; 10.1152/ajpheart.00629.2003.-We evaluated the influence of chronic hypertriglyceridemia and endothelial dysfunction on myocardial glucose uptake (MGU) in Type 2 diabetic patients without coronary heart disease. Patients were divided into two groups according to fasting triglyceride (TG) levels: 5.4 Ϯ 1.1 and 1.5 Ϯ 0.3 mmol/l for high-and normal-TG groups, respectively. Five subjects were assigned to the high-TG group and 11 to the normal-TG group. Age, gender, body mass index, systolic and diastolic blood pressure, glucose, insulin, HbA1c, cholesterol, and HDL cholesterol were similar in the two groups, whereas free fatty acid (FFA) levels were higher in the high-TG group basally and at the end of the clamp. Furthermore, five healthy subjects were subjected to the same protocol and used as the control group. MGU was assessed by using 18 F-labeled 2-fluoro-2-deoxy-D-glucose under hyperglycemic-hyperinsulinemic conditions. Basal endothelin-1 and nitric oxide levels were significantly higher in the high-TG group than in the normal-TG and control groups, and cGMP and maximal postischemic vasodilation were significantly decreased in the high-TG group compared with the normal-TG and control groups. However, significant alterations were found in the same parameters in the normal-TG group compared with the control group. By the end of the hyperglycemic clamp, in the high-TG group, MGU was ϳ40 and 65% of that in the normal-TG and control groups. MGU negatively correlated with TG, FFA, and endothelin-1, whereas a positive correlation was found with cGMP and maximal postischemic vasodilation. In conclusion, increased TG and FFA levels are risks, in addition to Type 2 diabetes mellitus, for myocardial insulin resistance, endothelial dysfunction, and alteration of nitric oxide/cGMP levels. triglycerides; myocardial glucose uptake; positron emission tomography study; endothelium; free fatty acid FOR MANY YEARS, hypertriglyceridemia was considered a marker of cardiovascular disease only in certain subjects, such as women (5, 12) and patients with Type 2 diabetes (10). The association between triglycerides (TGs), independently of HDL cholesterol levels, and definite cardiovascular disease, such as myocardial infarction or angina, was found in some studies (5) and denied in others, in which the simultaneous association of high TG and low HDL cholesterol was necessary to predict cardiovascular risk (8). This apparent discrepancy is probably related to the fact that it is quite difficult to match for duration and degree of cardiovascular disease in different populations, and, when cardiovascular disease is established, some factors might have lost their primary pathogenic significance. Hypertriglyceridemia occurs frequently in patients with coronary heart disease (CHD) and in survivors of myocardial infarction (5), and, durin...

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Section: Effects Of Type 2 Diabetes Mellitus On Myocardial Insulin Rementioning

confidence: 99%

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Monti¹,

Landoni²,

Setola³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Vascular endothelial cells secrete both ET-1 and big ET-1 (35). Both peptides are detected in plasma from healthy individuals and increase during, e.g., myocardial infarction (30). The potent and prolonged vasoconstriction in the splanchnic, renal, and pulmonary vascular beds has previously been demonstrated in healthy young individuals during systemic infusion of both ET-1 (39,40) or its precursor big ET-1 (3,4).…”

mentioning

confidence: 93%

“…Elevated plasma ET-1 levels have been demonstrated in virtually all diseases involving the cardiovascular or pulmonary systems, such as in patients with, e.g., myocardial infarction (30), atherosclerosis (26), systemic (33) and pulmonary (36) hypertension, and diabetes (38).…”

mentioning

confidence: 99%

Insulin sensitivity and big ET-1 conversion to ET-1 after ET_A- or ET_B-receptor blockade in humans

Ahlborg

Lindstrøm

2002

Journal of Applied Physiology

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Ahlborg, Gunvor, and Jonas Lindströ m. Insulin sensitivity and big ET-1 conversion to ET-1 after ETA-or ETBreceptor blockade in humans. J Appl Physiol 93: 2112-2121, 2002. First published September 6, 2002 10.1152/japplphysiol.00477.2002-Cardiovascular diseases are characterized by insulin resistance and elevated endothelin (ET)-1 levels. Furthermore, ET-1 induces insulin resistance. To elucidate this mechanism, six healthy subjects were studied during a hyperinsulinemic euglycemic clamp during infusion of (the ET-1 precursor) big ET-1 alone or after ETA-or ETB-receptor blockade. Insulin levels rose after big ET-1 with or without the ETB antagonist BQ-788 (P Ͻ 0.05) but were unchanged after the ETA antagonist BQ-123 ϩ big ET-1. Infused glucose divided by insulin fell after big ET-1 with or without BQ-788 (P Ͻ 0.05). Insulin and infused glucose divided by insulin values were normalized by ETA blockade. Mean arterial blood pressure rose during big ET-1 with or without BQ-788 (P Ͻ 0.001) but was unchanged after BQ-123. Skeletal muscle, splanchnic, and renal blood flow responses to big ET-1 were abolished by BQ-123. ET-1 levels rose after big ET-1 (P Ͻ 0.01) in a similar way after BQ-123 or BQ-788, despite higher elimination capacity after ETA blockade. In conclusion, ET-1-induced reduction in insulin sensitivity and clearance as well as splanchnic and renal vasoconstriction are ETA mediated. ETA-receptor stimulation seems to inhibit the conversion of big ET-1 to ET-1. skeletal muscle; splanchnic blood flow; renal blood flow; mean arterial blood pressure ENDOTHELIN (ET)-1 WAS CHARACTERIZED as well as the gene encoding for the prepropeptide cloned by Yanagisawa et al. (42). ET-1 belongs to a family of vasoactive peptides and is synthesized by the endothelium from its inactive precursor, big ET-1. Vascular endothelial cells secrete both ET-1 and big ET-1 (35). Both peptides are detected in plasma from healthy individuals and increase during, e.g., myocardial infarction (30). The potent and prolonged vasoconstriction in the splanchnic, renal, and pulmonary vascular beds has previously been demonstrated in healthy young individuals during systemic infusion of both ET-1 (39, 40) or its precursor big ET-1 (3, 4). Both big ET-1 and ET-1 are efficiently eliminated in the splanchnic, renal, and skeletal muscle vascular beds (4, 21, 39, 40), and ET-1 is eliminated in the pulmonary circulation as well (40). At a given arterial ET-1 level, the vascular responses to infused big ET-1 are more pronounced than to ET-1 infusion (3, 4), indicating that locally synthesized ET-1 reaches more vascular smooth muscle ET-1 receptors than ET-1 taken up from the blood.The vascular responses can be explained by the presence of two different ET-receptor subtypes: ET A and ET B (8, 34). ET A and ET B are found on vascular smooth muscle cells where both mediate contraction (12, 15), whereas only ET B receptors are located on the endothelial cells and stimulate the production of the vasodilators prostacyclin (16) and nitric oxide (NO) (16,28). ...

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“…Miyauchi et al (14) and others (12,16,(28)(29)(30) has been reported that plasma concentration of ET-1(1-21) in patients with acute myocardial infarction significantly rose after an attack and gradually decreased, and returned to the normal level in approximately two weeks. Furthermore, plasma concentrations of ET-1(1-21) rose after laparotomy and thoracotomy (31), coronary artery bypass grafting (32), and PTCA (33,34), and these values were gradually normalized after surgery.…”

Section: Discussionmentioning

confidence: 94%

A novel peptide of endothelin family, 31 amino-acid length endothelin in patients with acute myocardial infarction

et al. 2014

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Increased Plasma Concentrations of Endothelin-1 and Big Endothelin-1 in Acute Myocardial Infarction

Cited by 544 publications

References 8 publications

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Insulin sensitivity and big ET-1 conversion to ET-1 after ET_A- or ET_B-receptor blockade in humans

A novel peptide of endothelin family, 31 amino-acid length endothelin in patients with acute myocardial infarction

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Increased Plasma Concentrations of Endothelin-1 and Big Endothelin-1 in Acute Myocardial Infarction

Cited by 544 publications

References 8 publications

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Insulin sensitivity and big ET-1 conversion to ET-1 after ETA- or ETB-receptor blockade in humans

A novel peptide of endothelin family, 31 amino-acid length endothelin in patients with acute myocardial infarction

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Insulin sensitivity and big ET-1 conversion to ET-1 after ET_A- or ET_B-receptor blockade in humans