Inhibitory Effect of Epidermal Growth Factor and Hepatocyte Growth Factor on Endothelin-1 Release by Rabbit Proximal Tubule Cells

Haug, Cornelia; Linder, Theresia; Schmid‐Kotsas, Alexandra; Hetzel, Simone; Ernst, Friedlinde; Gruenert, Adolf; Jehle, Peter

doi:10.1097/00005344-200036051-00073

Cited by 3 publications

(2 citation statements)

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“…4); however, the identified modulators appear to be primarily activated under pathophysiological conditions. For example, following renal injury, epidermal growth factor (EGF) and hepatocyte growth factor (HGF), most likely via activation of receptor tyrosine kinase activity, inhibit basal and calcineurin inhibitor-stimulated cultured rabbit PT ET-1 release (269). Acute hypoxia increases PT ET-1 immunostaining (537).…”

Section: Endothelin and The Kidneymentioning

confidence: 99%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

373

459

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Endothelin (ET) peptides and their receptors are intimately involved in the physiological control of systemic blood pressure and body Na homeostasis, exerting these effects through alterations in a host of circulating and local factors. Hormonal systems affected by ET include natriuretic peptides, aldosterone, catecholamines, and angiotensin. ET also directly regulates cardiac output, central and peripheral nervous system activity, renal Na and water excretion, systemic vascular resistance, and venous capacitance. ET regulation of these systems is often complex, sometimes involving opposing actions depending on which receptor isoform is activated, which cells are affected, and what other prevailing factors exist. A detailed understanding of this system is important; disordered regulation of the ET system is strongly associated with hypertension and dysregulated extracellular fluid volume homeostasis. In addition, ET receptor antagonists are being increasingly used for the treatment of a variety of diseases; while demonstrating benefit, these agents also have adverse effects on fluid retention that may substantially limit their clinical utility. This review provides a detailed analysis of how the ET system is involved in the control of blood pressure and Na homeostasis, focusing primarily on physiological regulation with some discussion of the role of the ET system in hypertension.

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Section: Endothelin and The Kidneymentioning

confidence: 99%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

373

459

View full text Add to dashboard Cite

show abstract

“…The only agents shown to inhibit PT ET-1 release are epidermal growth factor (EGF) and hepatocyte growth factor (HGF), factors typically associated with renal injury (151). In contrast, a variety of substances and conditions associated with renal injury or inflammation enhance PT ET-1 production, including hypoxia (305), thrombin, transforming growth factor-ß (TGF-ß), TNF-α and IL-1ß (308).…”

Section: Et and Sodium Transportmentioning

confidence: 99%

Physiology of Endothelin and the Kidney

Kohan

Inscho

Wesson

et al. 2011

Comprehensive Physiology

104

136

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Since its discovery in 1988 as an endothelial cell-derived peptide that exerts the most potent vasoconstriction of any known endogenous compound, endothelin (ET) has emerged as an important regulator of renal physiology and pathophysiology. This review focuses on how the ET system impacts renal function in health; it is apparent that ET regulates multiple aspects of kidney function. These include modulation of glomerular filtration rate and renal blood flow, control of renin release, and regulation of transport of sodium, water, protons and bicarbonate. These effects are exerted through ET interactions with almost every cell type in the kidney, including mesangial cells, podocytes, endothelium, vascular smooth muscle, every section of the nephron, and renal nerves. In addition, while not the subject of the current review, ET can also indirectly affect renal function through modulation of extrarenal systems, including the vasculature, nervous system, adrenal gland, circulating hormones and the heart. As will become apparent, these pleiotropic effects of ET are of fundamental physiologic importance in the control of renal function in health. In addition, to help put these effects into perspective, we will also discuss, albeit to a relatively limited extent, how alterations in the ET system can contribute to hypertension and kidney disease.

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Endothelin-A receptor blockade slows the progression of renal injury in experimental renovascular disease

Kelsen

Hall

Chade

2011

American Journal of Physiology-Renal Physiology

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Endothelin (ET)-1, a potent renal vasoconstrictor with mitogenic properties, is upregulated by ischemia and has been shown to induce renal injury via the ET-A receptor. The potential role of ET-A blockade in chronic renovascular disease (RVD) has not, to our knowledge, been previously reported. We hypothesized that chronic ET-A receptor blockade would preserve renal hemodynamics and slow the progression of injury of the stenotic kidney in experimental RVD. Renal artery stenosis, a major cause of chronic RVD, was induced in 14 pigs and observed for 6 wk. In half of the pigs, chronic ET-A blockade was initiated (RVD+ET-A, 0.75 mg·kg(-1)·day(-1)) at the onset of RVD. Single-kidney renal blood flow, glomerular filtration rate, and perfusion were quantified in vivo after 6 wk using multidetector computer tomography. Renal microvascular density was quantified ex vivo using three-dimensional microcomputer tomography, and growth factors, inflammation, apoptosis, and fibrosis were determined in renal tissue. The degree of stenosis and increase in blood pressure were similar in RVD and RVD+ET-A pigs. Renal hemodynamics, function, and microvascular density were decreased in the stenotic kidney but preserved by ET-A blockade, accompanied by increased renal expression of vascular endothelial growth factor, hepatocyte growth factor, and downstream mediators such as phosphorilated-Akt, angiopoietins, and endothelial nitric oxide synthase. ET-A blockade also reduced renal apoptosis, inflammation, and glomerulosclerosis. This study shows that ET-A blockade slows the progression of renal injury in experimental RVD and preserves renal hemodynamics, function, and microvascular density in the stenotic kidney. These results support a role for ET-1/ET-A as a potential therapeutic target in chronic RVD.

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Inhibitory Effect of Epidermal Growth Factor and Hepatocyte Growth Factor on Endothelin-1 Release by Rabbit Proximal Tubule Cells

Cited by 3 publications

References 0 publications

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Physiology of Endothelin and the Kidney

Endothelin-A receptor blockade slows the progression of renal injury in experimental renovascular disease

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