Human Urotensin II as a Link between Hypertension and Coronary Artery Disease

Watanabe, Takuya; Kanome, Tomoko; Miyazaki, Akira; Kubo, Takashi

doi:10.1291/hypres.29.375

Cited by 63 publications

(53 citation statements)

References 108 publications

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“…The acute calcium influx through TRPC3 channels is a key signaling mechanism that stimulates the calcium-dependent release of several endothelium-derived vasoconstrictive agents including endothelin, urotensin, or epoxyeicosatrienoic acids. [12][13][14] In conclusion for the first time we observed direct evidence that TRPC3 expression in human vascular endothelium is associated with malignant hypertension.…”

Section: Discussionmentioning

confidence: 53%

Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

et al. 2009

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An increased expression of transient receptor potential canonical type 3 (TRPC3) cation channels has been proposed as one of the factors contributing to the pathogenesis of hypertension. To test that hypothesis we compared the expression of TRPC3 and TRPC6 as an endogenous control in human vascular endothelium of preglomerular arterioles in kidney biopsies from six patients with malignant hypertension and from four patients with diarrhea-associated hemolytic-uremic syndrome. Patients with malignant hypertension showed significantly higher systolic blood pressure and more prominent expression of TRPC3 in vascular endothelium of preglomerular arterioles compared to patients with hemolytic-uremic syndrome. The expression of TRPC6 was not different between the two groups. The study supports the hypothesis that the increased expression of TRPC3 is associated with malignant hypertension in humans. Malignant hypertension is a hypertensive emergency with severe elevation of blood pressure, a Keith-Wagener-Barker grade III or IV hypertensive retinopathy, and acute impairment of renal function in most cases. In white subjects, essential hypertension accounts for approximately 30% of malignant hypertension, whereas in blacks essential hypertension is the predominant cause, accounting for approximately 82% of all cases. The characteristic pathological change of malignant hypertension represents endothelial injury. Its pathophysiology involves mechanical stress on the vessel wall, a proliferative endarteriitis in small arteries and arterioles, and fibrinoid necrosis with fine subendothelial droplets and hyalin thrombi formation.

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Section: Discussionmentioning

confidence: 53%

Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

et al. 2009

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“…Experimental evidence points to Ca 2ϩ release via PLC/dependent IP 3 and calmodulin-dependent myosin light-chain kinase pathways, with ERK and RhoA/Rho kinase pathways also partially involved. The latter two pathways are also important in VSMC proliferation and migration (138). The endothelium-dependent vasodilatory effects of UII occur through the release of NO, prostaglandin E 2 , and endothelium-derived hyperpolarizing factor (94,138) (Fig.…”

mentioning

confidence: 99%

Role of urotensin II in health and disease

Ross

McKendy

Giaid

2010

American Journal of Physiology-Regulatory, Integrative and Comp

128

107

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Urotensin II (UII) is an 11 amino acid cyclic peptide originally isolated from the goby fish. The amino acid sequence of UII is exceptionally conserved across most vertebrate taxa, sharing structural similarity to somatostatin. UII binds to a class of G protein-coupled receptor known as GPR14 or the urotensin receptor (UT). UII and its receptor, UT, are widely expressed throughout the cardiovascular, pulmonary, central nervous, renal, and metabolic systems. UII is generally agreed to be the most potent endogenous vasoconstrictor discovered to date. Its physiological mechanisms are similar in some ways to other potent mediators, such as endothelin-1. For example, both compounds elicit a strong vascular smooth muscle-dependent vasoconstriction via Ca 2ϩ release. UII also exerts a wide range of actions in other systems, such as proliferation of vascular smooth muscle cells, fibroblasts, and cancer cells. It also 1) enhances foam cell formation, chemotaxis of inflammatory cells, and inotropic and hypertrophic effects on heart muscle; 2) inhibits insulin release, modulates glomerular filtration, and release of catecholamines; and 3) may help regulate food intake and the sleep cycle. Elevated plasma levels of UII and increased levels of UII and UT expression have been demonstrated in numerous diseased conditions, including hypertension, atherosclerosis, heart failure, pulmonary hypertension, diabetes, renal failure, and the metabolic syndrome. Indeed, some of these reports suggest that UII is a marker of disease activity. As such, the UT receptor is emerging as a promising target for therapeutic intervention. Here, a concise review is given on the vast physiologic and pathologic roles of UII.UT receptor; somatostatin; human; experimental animals; autocrine/paracrine UROTENSIN II (UII) was initially isolated from the urophysis of the goby fish (Gillichthys mirabilis) (97). The peptide was subsequently isolated from the white sucker (Catostomus commersoni) and the carp (Cyprinus carpio). Although there were variations in the amino acid sequence near the amino terminus, in both species the UII molecule retained the COOH-terminal cyclic sequence: -Cys

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“…Urotensin-II, an endogenous vasoconstrictor, has been suggested to be involved in the pathogenesis of vascular endothelial dysfunction (VED) (Maguire, J.J., 2002). Urotensin-II increases the activity of NADPH oxidase and plasminogen activator inhibitor-1 (PAI-1) and cause decrease in endothelium dependent relaxation (Watanabe, T., 2006). The overexpression of urotensin-II in endothelial cells cause VED by increasing the expression of type 1 collagen and formation of ROS.…”

Section: Urotensinmentioning

confidence: 99%