Renal actions of endothelin: Linking cellular signaling pathways to kidney disease

Marsen, Tobias A.; Schramek, Herbert; Dünn, Michael J.

doi:10.1038/ki.1994.43

Cited by 82 publications

(36 citation statements)

References 77 publications

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“…Interestingly, the use of selective COX-2 inhibitors is associated with an increased risk of acute renal failure, although the exact mechanisms are unknown (2). Endothelin-1 (ET-1) is a 21-amino acid peptide best known for its potent vasoconstrictor properties with probable contributions to renal inflammatory disease like glomerulonephritis (3,4). Additionally, ET-1 induces the expression of COX-2 in rat mesangial cells (RMC) (5).…”

Section: Selective Inhibition Of Cyclooxygenase-2 (Cox-2)mentioning

confidence: 99%

Alterations in Subcellular Localization of p38 MAPK Potentiates Endothelin-stimulated COX-2 Expression in Glomerular Mesangial Cells

Pratt

Bokemeyer

Foschi

et al. 2003

Journal of Biological Chemistry

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Section: Selective Inhibition Of Cyclooxygenase-2 (Cox-2)mentioning

confidence: 99%

Alterations in Subcellular Localization of p38 MAPK Potentiates Endothelin-stimulated COX-2 Expression in Glomerular Mesangial Cells

Pratt

Bokemeyer

Foschi

et al. 2003

Journal of Biological Chemistry

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“…High abundance of ET A receptors has been detected in the aorta, heart, and kidney, whereas ET B receptors are expressed mainly in the endothelium and tubular epithelial cells of the collecting duct (24,25,26,40). Activation of ET A receptors on vascular smooth muscle cells (VSMC) increases intracellular Ca 2ϩ levels, leading to prolonged vasoconstriction and cell proliferation (31,35,41). In contrast, activation of ET B receptors, present on endothelial cells, induces the release of nitric oxide (NO) and prostaglandins, thus provoking transient vasodilation (41,43,44).…”

mentioning

confidence: 99%

Adverse effects of pneumoperitoneum on renal function: involvement of the endothelin and nitric oxide systems

Abassi

Bishara²,

Karram³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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The mechanism underlying this phenomenon is largely unknown. This study was designed to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO) systems in IAP-induced renal dysfunction. Rats were subjected to IAP of 14 mmHg for 1 h, followed by a deflation for 60 min (recovery). Four additional groups were pretreated with 1) ABT-627, an ET A antagonist; 2) A-192621, an ETB antagonist; 3) nitroglycerine; and 4) N G -nitro-L-arginine methyl ester, a NO synthase inhibitor, before IAP. Urine flow rate (V), absolute Na ϩ excretion (UNaV), glomerular filtration rate (GFR), and renal plasma flow (RPF) were determined. Significant reductions in kidney function and hemodynamics were observed when IAP was applied. V decreased from 8.1 Ϯ 1.0 to 5.8 Ϯ 0.5 l/min, UNaV from 1.08 Ϯ 0.31 to 0.43 Ϯ 0.10 eq/min, GFR from 1.84 Ϯ 0.12 to 1.05 Ϯ 0.06 ml/min (Ϫ46.9 Ϯ 2.7% from baseline), and RPF from 8.62 Ϯ 0.87 to 3.82 Ϯ 0.16 ml/min (Ϫ54 Ϯ 3.5% from baseline). When the animals were pretreated with either ABT-627 or A-192621, given alone or combined, the adverse effects of IAP on GFR, RPF, V, and UNaV were significantly augmented. When the animals were pretreated with nitroglycerine, the adverse effects of pneumoperitoneum on GFR and RPF were substantially improved. In contrast, pretreatment with N G -nitro-L-arginine methyl ester remarkably aggravated pneumoperitoneum-induced renal dysfunction. In conclusion, decreased renal excretory function and hypofiltration are induced by increased IAP. These effects are related to impairment of renal hemodynamics and could be partially ameliorated by pretreatment with nitroglycerine and aggravated by NO and ET blockade.rat; intra-abdominal pressure PNEUMOPERITONEUM AT PRESSURE above 10 mmHg during laparoscopic surgery has been shown to produce transient oliguria and reduced glomerular filtration rate (GFR) and renal blood flow (RBF) (3,9,16,33,34). Despite much research in this field, the systemic physiological consequences of CO 2 pneumoperitoneum and the mechanisms underlying its adverse effects on renal hemodynamics and excretory function are not fully understood (9). However, there is compelling experimental evidence that the adverse renal effects induced by pneumoperitoneum are affected by the level of intra-abdominal pressure (IAP), volume status, degree of hypercarbia, positioning, and individual hemodynamic and renal reserves (9, 10). Additional factors that may affect renal function during pneumoperitoneum include direct compression of the renal parenchyma and renal vein (4, 17), increased resistance in the renal vasculature (47), and release of vasoconstrictors, such as vasopressin, angiotensin II, catecholamines, and endothelin (ET)-1 (1, 13). The latter is a very potent natural mammalian vasoconstrictor agent (25), acting on the cardiovascular and renal systems and other target organs by binding to two major types of receptors, ET A and ET B (2,25,36). High abundance of ET A receptors has been detected in the aorta, heart, and kidney, whereas ET B receptors are expre...

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“…AntiAng II treatment associated with decreased expressions of endogenous Ang II and iNOS found in this study could induce decreased vasopressor effects. In addition, Ang II is capable of inducing endothelin-1 production (Touyz and Schiffrin, 2003), a more powerful vasoconstrictor (Kon and Badr, 1991;Marsen et al, 1994); in this case, decreased Ang II activity could lead to decreased ET-1, and this could represent a beneficial status during this nephropathy. Via the AT1 receptor, angiotensin II also stimulates IL-6 production by vascular smooth muscle cells (Funakoshi et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

Peña

Hernández-Fonseca

Rincón

et al. 2012

Journal of Immunotoxicology

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Renal actions of endothelin: Linking cellular signaling pathways to kidney disease

Cited by 82 publications

References 77 publications

Alterations in Subcellular Localization of p38 MAPK Potentiates Endothelin-stimulated COX-2 Expression in Glomerular Mesangial Cells

Alterations in Subcellular Localization of p38 MAPK Potentiates Endothelin-stimulated COX-2 Expression in Glomerular Mesangial Cells

Adverse effects of pneumoperitoneum on renal function: involvement of the endothelin and nitric oxide systems

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

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