Angiotensin II enhances endothelin-1-induced vasoconstriction through upregulating endothelin type A receptor

Lin, Yan-Jie; Kwok, Ching Fai; Juan, Chi Chang; Hsu, Yung-Pei; Shih, KC; Chen, Chin-Chang; Ho, ­Low‐Tone

doi:10.1016/j.bbrc.2014.07.119

Cited by 57 publications

(35 citation statements)

References 22 publications

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“…Infusion of these agonistic antibodies into pregnant rats induces hypertension that is associated with an 11-fold increase in renal and a four-fold increase in placental expression of preproET-1 mRNA levels [10]. This increased expression of ET-1 is mediated by activation of the angiotensin II type-1 receptor as it can be blocked by losartan [11].…”

Section: Elevated Endothelin In Preeclampsiamentioning

confidence: 98%

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Saleh

Danser

Meiracker

2016

Current Opinion in Nephrology and Hypertension

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Section: Elevated Endothelin In Preeclampsiamentioning

confidence: 98%

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Saleh

Danser

Meiracker

2016

Current Opinion in Nephrology and Hypertension

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“…In particular, in several autoimmune disorders, such as systemic sclerosis and systemic lupus erythematosus, the presence of PAH has been associated with the existence of autoantibodies directed against ET A R (and against AT 1 R in the case of systemic sclerosis) . In addition, endothelin‐1 and angiotensin II are two of the most potent vasoconstrictors with a synergistic effect on the development of blood hypertension . Further, autoantibodies directed against ET A R and against AT 1 R are elevated in patients with end‐stage CF , the ultimate cause of the lung disease in our patient.…”

Section: Discussionmentioning

confidence: 66%

Immediate and Catastrophic Antibody-Mediated Rejection in a Lung Transplant Recipient With Anti–Angiotensin II Receptor Type 1 and Anti–Endothelin-1 Receptor Type A Antibodies

Calabrese

Schiavon

Feltracco

et al. 2017

American Journal of Transplantation

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Preexisting donor-specific anti-HLA antibodies (DSAs) have been associated with reduced survival of lung allografts. However, antibodies with specificities other than HLA may have a detrimental role on the lung transplant outcome. A young man with cystic fibrosis underwent lung transplantation with organs from a suitable deceased donor. At the time of transplantation, there were no anti-HLA DSAs. During surgery, the patient developed a severe and intractable pulmonary hypertension associated with right ventriular dysfunction, which required arteriovenous extracorporeal membrane oxygenation. After a brief period of clinical improvement, a rapid deterioration in hemodynamics led to the patient's death on postoperative day 5. Postmortem studies showed that lung specimens taken at the end of surgery were compatible with antibody-mediated rejection (AMR), while terminal samples evidenced diffuse capillaritis, blood extravasation, edema, and microthrombi, with foci of acute cellular rejection (A3). Immunological investigations demonstrated the presence of preexisting antibodies against the endothelin-1 receptor type A (ETA R) and the angiotensin II receptor type 1 (AT1 R), two of the most potent vasoconstrictors reported to date, whose levels slightly rose after transplantation. These data suggest that preexisting anti-ETA R and anti-AT1 R antibodies may have contributed to the onset of AMR and to the catastrophic clinical course of this patient

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“…The RAAS, ET-1 and NO interact in a complex fashion (Figure 3) [90]: Ang II was shown to stimulate the expression or release of ET-1 in endothelial cells in vitro, and to increase ET-1 production in the kidney [22,91]. It also up-regulates the expression of the ETA receptor [92] and the binding of ET-1 to this receptor in endothelial cells in vitro [93], and in the kidney in vivo. In contrast to Ang II, which whilst constricting all intra-renal vessels has its most prominent effects on the post-glomerular vessels, ET-1 causes mainly pre-glomerular constriction (Figure 4) [62].…”

Section: Interactions Between the Raas Et-1 And No In The Kidneymentioning

confidence: 99%

Endothelial factors in the pathogenesis and treatment of chronic kidney disease Part I

Rossi

Seccia

Barton

et al. 2018

Journal of Hypertension

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: Kidney damage is a common consequence of arterial hypertension, but is also a cause of atherogenesis. Dysfunction and/or harm of the endothelium in glomeruli and tubular interstitium damage the function of these structures and translates into dynamic changes of filtration fraction, with progressive reduction in glomerular filtration rate, expansion of extracellular fluid volume, abnormal ion balance, and hypoxia, ultimately leading to chronic kidney disease. Considering the key role played by endothelial dysfunction in chronic kidney disease, the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension and the Japanese Society of Hypertension have critically reviewed available knowledge on the mechanisms underlying endothelial cell injury. This resulted into two articles: in the first, we herein examine the mechanisms by which endothelial factors induce vascular remodeling and the role of different players, including endothelin-1, the renin-angiotensin-aldosterone system and their interactions, and of oxidative stress; in the second, we discuss the role of endothelial dysfunction in the major disease conditions that affect the kidney.

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Angiotensin II enhances endothelin-1-induced vasoconstriction through upregulating endothelin type A receptor

Cited by 57 publications

References 22 publications

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Immediate and Catastrophic Antibody-Mediated Rejection in a Lung Transplant Recipient With Anti–Angiotensin II Receptor Type 1 and Anti–Endothelin-1 Receptor Type A Antibodies

Endothelial factors in the pathogenesis and treatment of chronic kidney disease Part I

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