Endothelins in the urinary tract

Sullivan, M.; Mumtaz, Faiz; Khan, Masood; Dashwood, Michael R.; Thompson, CS; Mikhailidis, DP; Morgan, Robert J.

doi:10.1046/j.1464-410x.2000.00730.x

Cited by 22 publications

(7 citation statements)

References 98 publications

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“…The K d and B max of 125 I-ET-1 were similar in both normal and tumor homogenates. These figures are closely matched to previously published data regarding the characteristics of ET-1 binding in other tissues (30,31,32).…”

Section: Discussionsupporting

confidence: 91%

“…Similar alterations in receptor expression have been reported in autoradiographic studies on prostate and ovarian cancer (3,4). 125 I-ET-1 binding to vascular regions, shown here by colocalization with ET B -expressing endothelial cells and its known association with ET A -expressing vascular smooth muscle cells (30,31), highlights ET-1 angiogenic actions, such as VEGF production (33).…”

Section: Discussionmentioning

confidence: 68%

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Efficacy of the Specific Endothelin A Receptor Antagonist Zibotentan (ZD4054) in Colorectal Cancer: A Preclinical Study

Haque

Dashwood

Heetun

et al. 2013

Molecular Cancer Therapeutics

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Endothelin 1 (ET-1) is overexpressed in cancer, contributing to disease progression. We previously showed that ET-1 stimulated proliferative, migratory, and contractile tumorigenic effects via the ET A receptor. Here, for the first time, we evaluate zibotentan, a specific ET A receptor antagonist, in the setting of colorectal cancer, in cellular models. Pharmacologic characteristics were further determined in patient tissues. Colorectal cancer lines (n ¼ 4) and fibroblast strains (n ¼ 6), isolated from uninvolved areas of colorectal cancer specimens, were exposed to ET-1 and/or ET A/B receptor antagonists. Proliferation (methylene blue), migration (scratch wounds), and contraction (gel lattices) were assessed. Receptor distribution and binding characteristics (K d , B max ) were determined using autoradiography on tissue sections and homogenates and cytospun cells, supported by immunohistochemistry. Proliferation was inhibited by ET A (zibotentan > BQ123; P < 0.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 68%

Efficacy of the Specific Endothelin A Receptor Antagonist Zibotentan (ZD4054) in Colorectal Cancer: A Preclinical Study

Haque

Dashwood

Heetun

et al. 2013

Molecular Cancer Therapeutics

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“…An apparent upregulation of ET A R expression was observed in colorectal cancer sections, due to the greater number of vessels and the higher density of ET A R associated with them. ET A Rs are known to be expressed predominantly by vascular smooth muscle cells, with ET B R expressed mainly by endothelial cells [24,25]. Vascular smooth muscle cells are known to use paracrine tumour-derived growth-promoting and survival factors for angiogenesis, including ET-1.…”

Section: Discussionmentioning

confidence: 99%

Altered endothelin receptor subtypes in colorectal cancer

Hoosein

Dashwood²,

Dawas³

et al. 2007

European Journal of Gastroenterology & Hepatology

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“…Endothelins Endothelin (ET) receptors were shown in the urethral smooth muscle and urothelium in various animals [115][116][117] . ET-1 subtype was demonstrated to cause urethral smooth muscle contractions via ET-A receptors in the rabbit [118,119] . However, human studies regarding endothelins and urethral function are lacking.…”

Section: Npymentioning

confidence: 98%

Pharmacologic Targets on the Female Urethra

Canda

Çınar²,

Turna

et al. 2008

Urol Int

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Introduction: This article reviews the mechanisms affecting contraction and relaxation of the urethra in order to establish a basis for current and future treatments for urinary incontinence in women. Material and Methods: A review of the English literature using MEDLINE was performed between 1970 and 2008 on female urethra pharmacology, urinary incontinence, and mechanisms involved in contraction and relaxation of the female human urethra. Results: α-Adrenoceptors (ARs) cause contraction and β-ARs cause relaxation. Use of selective α-agonist and β-AR blocker agents might have potential for the treatment of stress urinary incontinence. Tolerable doses of cholinergic agonists did not have significant effects on intraurethral pressure. Nitric oxide seems to be the major nonadrenergic-noncholinergic inhibitory transmitter causing relaxation. c-kit-positive interstitial cells seem to regulate urethral tone. The roles of adenosine triphosphate and carbon monoxide have not been fully investigated in humans. Neuropeptides function similarly to the urinary bladder. Prostanoids cause urethral contraction and relaxation depending on their subtypes. Serotonin enhances the strength of urethral sphincteric contractions. The Rho-kinase pathway also appears to be modulating smooth muscle contraction in the urethra. Conclusions: Understanding of the urethral function and pharmacology may lead to the development of promising new agents which might be useful in the management of urinary incontinence in women.

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Endothelins in the urinary tract

Cited by 22 publications

References 98 publications

Efficacy of the Specific Endothelin A Receptor Antagonist Zibotentan (ZD4054) in Colorectal Cancer: A Preclinical Study

Efficacy of the Specific Endothelin A Receptor Antagonist Zibotentan (ZD4054) in Colorectal Cancer: A Preclinical Study

Altered endothelin receptor subtypes in colorectal cancer

Pharmacologic Targets on the Female Urethra

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