Plasma endothelin in congestive heart failure: effect of the ACE inhibitor, fosinopril

Galatius-Jensen, Søren; Wroblewski, Henrik; Emmeluth, Claus; Bie, Peter; Haunsø, Stig; Kastrup, Jens

doi:10.1016/s0008-6363(96)00148-4

Cited by 61 publications

(14 citation statements)

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“…The neurohumoral axis is typically activated in the heart failure patient, and in this regard endothelin, a potent vasoconstrictor, may play an important pathogenic role in the progression of CHF. In this regard, plasma endothelin concentrations were found to be elevated at baseline in a group of 34 patients with moderately severe CHF (39). When this cohort of patients was given 12 weeks of fosinopril treatment, not only did exercise tolerance improve significantly but endothelin concentrations normalized.…”

Section: Congestive Heart Failurementioning

confidence: 86%

Fosinopril: Emerging Considerations and Implications for Angiotensin‐Converting Enzyme Inhibitor Therapy

Sica

Gehr

Kelleher

et al. 1998

Cardiovascular Drug Reviews

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Section: Congestive Heart Failurementioning

confidence: 86%

Fosinopril: Emerging Considerations and Implications for Angiotensin‐Converting Enzyme Inhibitor Therapy

Sica

Gehr

Kelleher

et al. 1998

Cardiovascular Drug Reviews

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“…Через 4 нед. лече-ния ЭЗВД увеличилась до 7,5 ± 2,9% (р<0,05 [7,8]. Для фозиноприла характерно меньшее количество побочных эффектов по сравнению с другими представителями этого класса лекарственных препаратов, в частности более редкое возникновение кашля, что позволяет рассчитывать на хорошую компла-ентность пациентов к лечению.…”

Section: результаты и обсуждениеunclassified

Antihypertensive and Vasoprotective Effects of Fosinoprile in Patients With Arterial Hypertension

Grigorieva¹,

Кузнецов²,

Koroleva³

et al. 2017

Med. sov.

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“…Accordingly, a study by Minamino et al (1997) found that ECE-1 may contribute to the process of injury-induced neointimal formation and atherosclerosis through increased production of ET-1, which could be blocked using the ECE-1 inhibitor phosphoramidon. Likewise, blocking the elevated ECE-1 expression levels in failing human hearts helps reduce elevated plasma ET-1 levels to normal values, which results in additional arterial vasodilatation, improved cardiac index, and decreased systemic and pulmonary vascular resistance (Galatius-Jensen et al, 1996).…”

Section: Targeting the Elevated Levels Of Et-1 In Pathologic Conditionsmentioning

confidence: 99%

Endothelin-1–Induced Endoplasmic Reticulum Stress in Disease

Jain

2013

J Pharmacol Exp Ther

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The accumulation of unfolded proteins in the endoplasmic reticulum (ER) represents a cellular stress induced by multiple stimuli and pathologic conditions. Recent evidence implicates endothelin-1 (ET-1) in the induction of placental ER stress in pregnancy disorders. ER stress has previously also been implicated in various other disease states, including neurodegenerative disorders, diabetes, and cardiovascular diseases, as has ET-1 in the pathophysiology of these conditions. However, to date, there has been no investigation of the link between ET-1 and the induction of ER stress in these disease states. Based on recent evidence and mechanistic insight into the role of ET-1 in the induction of placental ER stress, the following review attempts to outline the broader implications of ET-1-induced ER stress, as well as strategies for therapeutic intervention based around ET-1. Endoplasmic Reticulum StressThe endoplasmic reticulum (ER) is a multifunctional organelle involved in the synthesis, folding, and post-translational modification of membrane and secretory proteins. In addition, the ER also serves as a reservoir of calcium ions (Ca 21 ) (Zhang and Kaufman, 2008). In the ER lumen, Ca 21 is buffered by calcium-binding proteins. Many of these proteins also serve as molecular chaperones involved in the folding and quality control of ER proteins, and their functional activity alters with changes in Ca 21 concentration (Michalak et al., 1998). Growth factors, hormones, and stimuli that perturb cellular energy levels, nutrient availability, or redox status all affect ER calcium storage. Loss of ER Ca 21 homeostasis suppresses posttranslational modifications of proteins in the ER. As a result, misfolded proteins accumulate, provoking ER stress response pathways known collectively as the unfolded protein response (UPR) (Brostrom and Brostrom, 2003).The UPR is induced to restore ER homeostasis. It reduces the burden of new proteins entering the ER lumen through attenuation of translation, enhances the protein folding capacity by increasing ER chaperone proteins [glucose-regulated protein78 (GRP78) and GRP94] and folding enzymes, and promotes degradation of remaining unfolded or misfolded proteins through increased capacity of the cytosolic ubiquitin-proteasome system (Brostrom and Brostrom,

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Plasma endothelin in congestive heart failure: effect of the ACE inhibitor, fosinopril

Cited by 61 publications

References 0 publications

Fosinopril: Emerging Considerations and Implications for Angiotensin‐Converting Enzyme Inhibitor Therapy

Fosinopril: Emerging Considerations and Implications for Angiotensin‐Converting Enzyme Inhibitor Therapy

Antihypertensive and Vasoprotective Effects of Fosinoprile in Patients With Arterial Hypertension

Endothelin-1–Induced Endoplasmic Reticulum Stress in Disease

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