Role of endothelin in cardiovascular disease

Agapitov, Alexei V.; Haynes, William G.

doi:10.3317/jraas.2002.001

Cited by 154 publications

(125 citation statements)

References 182 publications

(238 reference statements)

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“…ET-1 levels are elevated in patients with essential hypertension with no other risk factors for atherosclerosis, and this may serve as markers of endothelial dysfunction in uncomplicated hypertension. 30 A study by Vaindirlis et al 18 supported the existence of endothelial dysfunction in uncomplicated hypertension by showing increased amount of ET-1 in the urine analysis of adult patients with WCH. 18 Hlubocka et al 14 showed not only increased ET-1 levels in uncomplicated hypertension but also a decrease in ET-1 levels after treatment with ACE inhibitors.…”

Section: Discussionmentioning

confidence: 99%

Endothelium and angiogenesis in white coat hypertension

et al. 2004

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Hypertensive patients are at particular risk of cardiovascular complications, possibly related to endothelial damage or dysfunction, or to abnormal angiogenesis. The aim of this study was to compare the risk conferred by white coat hypertension (WCH) vs sustained hypertension in the development of the endothelial dysfunction and abnormal angiogenesis by evaluating nitric oxide (NO ¼ NO 2 þ NO 3 ), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and E-selectin levels in plasma. The study group included 102 subjects, 34 with WCH (17 male and 17 female patients) aged 49711 years, 34 sustained hypertensives (HT) (15 male and 19 female patients) aged 47711 years and 34 normotensive control subjects (NT) (16 male and 18 female patients) aged 48710 years. WCH was defined as clinical hypertension and daytime ambulatory blood pressure less than 135/85 mmHg. The subjects were matched for age, gender, body mass index and the patients with smoking habit, dyslipidaemia, and diabetes mellitus were excluded from the study. The NO, ET-1, VEGF and E-selectin levels were analysed by ELISA technique. The WCH subjects had significantly higher levels of NO than the HT (41.6872.23 vs 32.1872.68 lmol/l; Po0.001) and significantly lower values than the NT (48.2474.29 lmol/l; Po0.001). ET-1 levels of the WCH group were significantly higher than the NT (8.1070.92 vs 5.9570.26 ng/ml; Po0.001) and significantly lower than the HT (11.4670.59 ng/ml; Po0.001). Considering with VEGF, the WCH group had significantly higher levels than the NT (195.88711.84 vs 146.26718.67 pg/ml; Po0.001), but the difference from the HT group was not significant (203.3577.48 pg/ml; P ¼ 0.062). E-selectin in the WCH group was significantly lower than the HT (4.7770.52 vs 8.4972.85; Po0.001), but the difference from the NT group was not significant (3.8670.67; P ¼ 0.077). Our data demonstrate that WCH is associated with endothelial dysfunction and abnormal angiogenesis. The degree of these changes is not as severe as observed in hypertensive population.

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Section: Discussionmentioning

confidence: 99%

Endothelium and angiogenesis in white coat hypertension

et al. 2004

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“…Additionally, Endothelin signaling has also been implicated in guiding migratory NC cell, which will contribute to the formation of the enteric nervous system (ENS) (Heanue and Pachnis, 2007). Endothelins are a family of peptides comprising potent vasoconstrictors, which are primaliry expressed by the endothelium (Agapitov and Haynes, 2002). NC cells, which invade the developing gut express Endothelin receptor type B (EDNRB), while Edn3 is expressed in the midgut and hindgut mesoderm as well as in the caecum and proximal colon (Barlow et al, 2003, Leibl et al, 1999.2.1) In mouse, mutations in Edn3 and EDNRB cause delayed migration of gut-destinated NC cells (Barlow et al, 2003;Lee et al, 2003;Ro et al, 2006).…”

Section: Guiding Signals-attractantsmentioning

confidence: 99%

Controlled levels of canonical Wnt signaling are required for neural crest migration

Maj

Künneke

Loresch

et al. 2016

Developmental Biology

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“…There are data suggesting that certain polymorphisms of the genes coding for ET-1 and ET receptors could be associated with chronic elevations in blood pressure. 48 In experimental animals with induced hypertension, ET A receptor blockade prevents vascular hypertrophy and attenuates left ventricular hypertrophy. 49 Hypertension develops in ET B knockout mice and blood pressure rises after ET B blockade in people.…”

Section: Essential Hypertensionmentioning

confidence: 99%

Endothelin Receptor Blockers in Cardiovascular Disease

Rich¹,

McLaughlin²

2003

Circulation

197

126

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Abstract-The endothelin (ET) system is comprised of 4 active ETs, with ET-1 being the predominant isoform in the cardiovascular system. Because of the potent vasoconstricting and mitogenic effects of ET-1 and its involvement in various cardiovascular diseases, blockade of the ET receptor has received considerable attention. ET receptor antagonism has been demonstrated to be beneficial in patients with pulmonary hypertension. The nonselective ET receptor antagonist bosentan improves exercise capacity and increases time to clinical worsening in patients with pulmonary arterial hypertension. Key Words: endothelin Ⅲ heart failure Ⅲ pulmonary heart disease T he endothelin (ET) system, like other vascular regulatory systems, consists of a parent peptide that undergoes enzymatic activation and exerts its biologic effects by modulating specific receptors. Of the 4 active ETs (ET 1 through 4), ET-1 is the predominant isoform in the cardiovascular system, which is generated through the cleavage of prepro ET-1 to big ET-1 and then to ET-1 by the action of ET-converting enzymes. ET-1 is found in endothelial cells and is released toward the vascular smooth muscle consistent with a paracrine role, but it is also produced by smooth muscle cells and cardiomyocytes. 1,2 ET-1 has vasoconstrictive and mitogenic effects, stimulates the production of growth factors such as vascular endothelial growth factor and basic fibroblast growth factor, and potentiates the effects of transforming growth factor-␤ and platelet-derived growth factor. 3-7 Chronic ET-1 stimulation can result in myocardial fibrosis and hypertrophy and vascular fibrosis with extracellular matrix proliferation. 8 In the lung, ET-1 is abundantly expressed in the pulmonary vasculature and appears to play an important role in the regulation of pulmonary vascular tone. 9 ET-1 is also produced in leukocytes where it influences the production of a wide range of cytokines in the inflammatory response. 10 ET is regulated in an autocrine fashion by physiochemical factors such as blood flow, pulsatile stretch, sheer stress, and pH. 11-13 Acute hypoxia leads to selective stimulation of the ET-1 gene and ET synthesis in the pulmonary vasculature. 14 ET-1 biosynthesis is also stimulated by low-density lipoprotein cholesterol and glucose, and thrombin. 15,16 Endogenous inhibitors of ET-1 synthesis include nitric oxide, prostacyclin, atrial natriuretic peptides, and estrogens. [17][18][19][20] ET-1 exerts its major vascular effects through activation of 2 distinct G protein coupled ET A and ET B receptors. ET A receptors are found in the medial smooth muscle layers of the blood vessels, and atrial and ventricular myocardium. 21 When stimulated, the ET A receptors induce vasoconstriction and cellular proliferation by increasing intracellular calcium.ET B receptors are localized on endothelial cells and, to some extent, smooth muscle cells and macrophages. 22 The activation of ET B receptors stimulates the release of nitric oxide and prostacyclin and prevents apoptosis. 23 Normally, t...

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Role of endothelin in cardiovascular disease

Cited by 154 publications

References 182 publications

Endothelium and angiogenesis in white coat hypertension

Endothelium and angiogenesis in white coat hypertension

Controlled levels of canonical Wnt signaling are required for neural crest migration

Endothelin Receptor Blockers in Cardiovascular Disease

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