Metabolism of Big endothelin-1 (1–38) and (22–38) in the human circulation in relation to production of endothelin-1 (1–21)

Hemsén, Anette; Ahlborg, Gunvor; Ottosson‐Seeberger, Astrid; Lundberg, Jan M.

doi:10.1016/0167-0115(94)00119-i

Cited by 92 publications

(53 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 21 patients with IPAH, elevated ET-1 levels correlated with right atrial pressure and pulmonary artery oxygen saturation [37]. It has been proposed that big ET-1 may be a more reliable indicator of activity of the ET-1 system, owing to a longer half-life and less tissue extraction [47]. RUBENS et al [43] found significantly elevated plasma ET-1 and big ET-1 levels in 16 patients with IPAH; plasma ET-1 and big ET-1 showed a significant positive correlation with pulmonary vascular resistance and mean pulmonary artery pressure, and a significant negative correlation with cardiac output and cardiac index and, hence, disease severity.…”

Section: Natriuretic Peptidesmentioning

confidence: 99%

Biomarkers in pulmonary hypertension

Warwick

Thomas²,

Yates³

2008

Eur Respir J

140

View full text Add to dashboard Cite

There have been significant recent advances in the understanding of the pathophysiology of pulmonary hypertension, and a growing number of therapeutic agents have become available to the treating physician. Traditional methods of diagnosing and monitoring this condition have comprised echocardiography and right heart catheterisation, in addition to functional measures, such as estimation of functional class and the 6-min walk test. An increasing number of biomarkers have been described that are elevated in pulmonary hypertension and which may assist the clinician in diagnosis and in the assessment of disease severity and response to treatment.The present article details the more important biomarkers, their potential applications and the evidence supporting their use.

show abstract

Section: Natriuretic Peptidesmentioning

confidence: 99%

Biomarkers in pulmonary hypertension

Warwick

Thomas²,

Yates³

2008

Eur Respir J

140

View full text Add to dashboard Cite

show abstract

“…21). ANOVA regarding RBF for all four clamp protocol data showed significant differences between protocols (P Ͻ 0.01, as well as interaction clamp ϫ time, P Ͻ 0.001).…”

Section: Hr Map Arterial Blood Glucose Arterial-hepatic Venous Andmentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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). ...

show abstract

“…ECEs hydrolyse big ET-1 to yield the active 21aa ET-1 [6]. Big ET-1 has a circulating half-life of "23min" compared with only "3.5 min" for ET-1 [9]. So, big ET-1 with its long half-life has been implicated as a more accurate indicator of the activation degree of the endothelin system [10].…”

mentioning

confidence: 99%

Evaluation of serum big endothelin-1 for the diagnosis and prediction of disease recurrence in breast cancer patients

Na¹,

Mohammad²,

Elkerm³

et al. 2013

J Cancer Res Ther

View full text Add to dashboard Cite

Metabolism of Big endothelin-1 (1–38) and (22–38) in the human circulation in relation to production of endothelin-1 (1–21)

Cited by 92 publications

References 16 publications

Biomarkers in pulmonary hypertension

Biomarkers in pulmonary hypertension

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

Evaluation of serum big endothelin-1 for the diagnosis and prediction of disease recurrence in breast cancer patients

Contact Info

Product

Resources

About

Metabolism of Big endothelin-1 (1–38) and (22–38) in the human circulation in relation to production of endothelin-1 (1–21)

Cited by 92 publications

References 16 publications

Biomarkers in pulmonary hypertension

Biomarkers in pulmonary hypertension

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

Evaluation of serum big endothelin-1 for the diagnosis and prediction of disease recurrence in breast cancer patients

Contact Info

Product

Resources

About

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