| First Author | Rautureau Y | Year | 2015 |
| Journal | Hypertension | Volume | 66 |
| Issue | 2 | Pages | 347-55 |
| PubMed ID | 26101346 | Mgi Jnum | J:377224 |
| Mgi Id | MGI:8275260 | Doi | 10.1161/HYPERTENSIONAHA.115.05168 |
| Citation | Rautureau Y, et al. (2015) Inducible human endothelin-1 overexpression in endothelium raises blood pressure via endothelin type A receptors. Hypertension 66(2):347-55 |
| abstractText | The mechanisms of blood pressure regulation by endothelin-1 produced by endothelial cells are complex and still unclear. Transgenic mice with endothelium-restricted human endothelin-1 (EDN1) overexpression presented vascular damage but no significant change in blood pressure, which could be because of adaptation to life-long exposure to elevated endothelin-1 levels. We now generated a tamoxifen-inducible endothelium-restricted EDN1 overexpressing transgenic mouse (ieET-1) using Cre/loxP technology. Sixteen days after tamoxifen treatment, ieET-1 mice presented >/=10-fold increase in plasma endothelin-1 (P<0.01) and >/=20 mm Hg elevation in systolic blood pressure (P<0.01), which could be reversed by atrasentan (P<0.05). Endothelin-1 overexpression did not cause vascular or kidney injury or changes in kidney perfusion or function. However, endothelin type A and B receptor expression was differentially regulated in the mesenteric arteries and the kidney. Our results demonstrate using this ieET-1 mouse model that 21 days of induction of endothelin-1 overexpression caused endothelin-1-dependent elevated blood pressure mediated by endothelin type A receptors. |
