Polar secretion of endothelin-1 by cultured endothelial cells.

Wagner, Oswald; Christ, Guenter; Wojta, Johann; Vierhapper, H.; Parzer, S; Nowotny, Peter; Schneider, Barbara; Waldhäusl, W.; Binder, Bernd R.

doi:10.1016/s0021-9258(18)41966-7

Cited by 558 publications

(43 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…29,30 Experimental studies have shown that 80% of ET-1 secretion is polarized toward the basolateral portion of the endothelial cells, suggesting that ET-1 acts mainly as an autocrine/paracrine factor having biologic effects. 31 Circulating ET-1 levels are below the threshold of 30 to 300 pmol/L needed to elicit most logic effects. However, circulating ET-1 levels are apparently only rough in-dicators of changes in ET-1 synthesis and secretion.…”

Section: Resultsmentioning

confidence: 99%

Significance of Plasma Nitric Oxide/Endothelial-1 Ratio for Prediction of Coronary Artery Disease

Kurita¹,

Matsui

Ishizuka

et al. 2005

Angiology

View full text Add to dashboard Cite

Vascular tone is regulated by vasodilators and vasoconstrictors. Endothelin-1 (ET-1) is the predominant vasoconstrictor peptide that constricts vascular smooth muscle, whereas nitric oxide (NO) is the primary vasodilator peptide that relaxes vascular smooth muscle. In this study, the authors examined whether NO/ET-1 ratio is a useful marker for detecting coronary artery disease (CAD), by comparison with evaluation based on vascular endothelial (VE) function. They measured plasma NOX and ET-1 by using ENO-200 and radioimmunoassay, in 38 subjects with normal (NL) coronary arteries (NL group; mean age, 60 +/-12 years) and 25 subjects with CAD (CAD group; mean age, 69 +/- 6 years). VE function (randomized endothelium-dependent [D] and endothelium-independent [I] VE function) was assessed by measuring brachial artery (BA) diameter by using high-resolution ultrasound (7.5 MHz). Soon after these procedures, symptom-limited exercise testing was performed. There were no statistically significant differences in serum lipid concentrations or VED function between the groups. However, the CAD group had a significantly lower NO/ET-1 ratio (1.2 +/- 1.1 vs 2.7 +/- 2.2, p < 0.01) and BA diameter after sublingual nitroglycerin (VEID function: 6 +/- 7% vs 10 +/- 4%, p < 0.05). As expected, the ST segment and treadmill exercise duration were significantly lower in the CAD group. Sensitivity and specificity for detecting CAD by plasma NO/ET-1 ratio (> or =2 .0) were 90% and 85%, respectively; sensitivity and specificity for detecting CAD by ST depression (> or =1 mm) were 80% and 78%, respectively. The present results suggest that plasma NO/ET-1 ratio is a useful biological marker for predicting CAD.

show abstract

Section: Resultsmentioning

confidence: 99%

Significance of Plasma Nitric Oxide/Endothelial-1 Ratio for Prediction of Coronary Artery Disease

Kurita¹,

Matsui

Ishizuka

et al. 2005

Angiology

View full text Add to dashboard Cite

show abstract

“…Endothelins (ETs) have a variety of biological effects in noncardiovascular tissues, and there is increasing evidence that ETs act locally rather than as circulating peptides. Endothelial cells in culture release ET-1, predominantly into the basolateral compartment (Wagner et al 1992), and no ECE-1 was detected in plasma. The presence of ECE-1 in the same cell or in close proximity to its substrates is required for ETs to be effective local mediators.…”

Section: Discussionmentioning

confidence: 97%

Cellular Distribution of Endothelin-converting Enzyme-1 in Human Tissues

Korth

Bohle

Corvol

et al. 1999

J Histochem Cytochem.

View full text Add to dashboard Cite

SUMMARY Endothelin-converting enzyme-1 (ECE-1) is the key enzyme of endothelin biosynthesis, catalyzing the final processing step. As shown by the targeted disruption of the ECE-1 gene, mature endothelins must be produced at specific sites for normal embryonic development. Therefore, it is important to know the exact pattern of ECE-1 gene expression. In this study we investigated the cellular distribution of ECE-1 in a variety of human tissues by in situ hybridization and immunohistochemistry. Widespread expression of the ECE-1 gene was noted, with a similar distribution pattern for mRNA and protein in normal human tissues, suggesting a major biological role for ECE-1. ECE-1 levels were particularly high in the cardiovascular, reproductive, and endocrine systems. There was strong and consistent labeling for ECE-1 in the vascular endothelial cells of all organs examined and in various nonvascular cells, especially some glandular cells. A large amount of ECE-1 protein and mRNA was detected in the Leydig cells of the testis and in the granulosa and theca cells of the ovary. In the adrenal gland, ECE-1 was detected in the cortex and medulla, with the strongest labeling in the zona glomerulosa. Therefore, ECE-1 may be involved in other systems, such as the regulation of hormone secretion, rather than exclusively generating ET-1 from its precursor. These results point out the potential side effects of ECE-1 inhibitors that are currently under development for treatment of cardiovascular diseases.

show abstract

“…14 Metabolic acidosis in subjects with low GFR might increase kidney ET-1 through acid-induced ET-1 release from kidney microvascular endothelium because an acid extracellular environment within the physiologic range increases ET-1 release from human kidney microvascular endothelium in vitro. 20 ET-1 release from vascular endothelium is predominantly basolateral 21 and so microvascular endothelium might add ET-1 to cortical interstitium adjacent to the interstitial space. 22 Cortical epithelium secretes and releases basolateral ET-1 23 and might also be a source of kidney cortical interstitial ET-1.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR

Phisitkul

Khanna

Simoni

et al. 2010

Kidney International

262

250

View full text Add to dashboard Cite

Metabolic acidosis often accompanies low glomerular filtration rate and induces secretion of endothelin, which in turn might mediate kidney injury. Here we tested whether treatment of metabolic acidosis in patients with low glomerular filtration rate reduced the progression of kidney disease. Fifty-nine patients with hypertensive nephropathy and metabolic acidosis had their blood pressure reduced with regimens that included angiotensin-converting enzyme inhibition. Thirty patients were then prescribed sodium citrate, and the remaining 29, unable or unwilling to take sodium citrate, served as controls. All were followed for 24 months with maintenance of their blood pressure reduction. Urine endothelin-1 excretion, a surrogate of kidney endothelin production, and N-acetyl-beta-D-glucosaminidase, a marker of kidney tubulointerstitial injury, were each significantly lower, while the rate of estimated glomerular filtration rate decline was significantly slower. The estimated glomerular filtration rate was statistically higher after 24 months of sodium citrate treatment compared to the control group. Hence it appears that sodium citrate is an effective kidney-protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition.

show abstract

Polar secretion of endothelin-1 by cultured endothelial cells.

Cited by 558 publications

References 20 publications

Significance of Plasma Nitric Oxide/Endothelial-1 Ratio for Prediction of Coronary Artery Disease

Significance of Plasma Nitric Oxide/Endothelial-1 Ratio for Prediction of Coronary Artery Disease

Cellular Distribution of Endothelin-converting Enzyme-1 in Human Tissues

Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR

Contact Info

Product

Resources

About