1999
DOI: 10.1016/s0014-2999(99)00447-1
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Cyclosporin A induces prepro endothelin-1 gene transcription in human endothelial cells

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Cited by 15 publications
(8 citation statements)
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“…[11][12][13] In this study, we found increased arterial levels of ET-1 in the transplant group, which is in accordance with previous reports. 11 However, during ET-A receptor blockade, ET-1 levels increased in the control group but remained unchanged in the transplant group ( Figure 4).…”
Section: Et-1 In Plasmasupporting
confidence: 93%
See 1 more Smart Citation
“…[11][12][13] In this study, we found increased arterial levels of ET-1 in the transplant group, which is in accordance with previous reports. 11 However, during ET-A receptor blockade, ET-1 levels increased in the control group but remained unchanged in the transplant group ( Figure 4).…”
Section: Et-1 In Plasmasupporting
confidence: 93%
“…[2][3][4] In the vasculature, CsA induces vasoconstriction, 9 impairs endothelial function, 10 and increases ET-1 synthesis. [11][12][13] ET-A receptor blocking agents reduce CsA-induced vasoconstriction in different animal models, 14 -17 but no human data have been reported.…”
mentioning
confidence: 99%
“…[40][41][42][43][44] Cyclosporine is also known to induce vasoconstriction through endothelial cell production and release of endothelin and systemic sympathetic stimulation. 43,[45][46][47] Systemic/renal vasoconstriction with resultant hypertension could lead to reduced cerebral blood flow due to autoregulatory vasoconstriction. In addition, these drugs could reduce cerebral blood flow directly, secondary to cerebral vasoconstriction.…”
Section: Associated Clinical Conditionsmentioning
confidence: 99%
“…Cyclosporine causes a rapid vasoconstriction of the preglomerular afferent arteriole resulting in a decreased blood flow and reduced glomerular filtration (5). Endothelin-1 (6,7), increased sympathetic tone (8,9), alterations in the prostaglandin-thromboxane cascade (10,11), NO-blockade (12,13), and angiotensin II (14 -16) all play a role in the development of these functional changes. Sustained renal ischemia and direct vascular endothelial and renal tubular cell toxicity leads to arteriolar hyalinization, tubular atrophy, interstitial fibrosis (TGF-␤1), and glomerulosclerosis (17).…”
mentioning
confidence: 99%