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Cardiac Emergencies in Obstetrics
Published in Sanjeewa Padumadasa, Malik Goonewardene, Obstetric Emergencies, 2021
Sanjeewa Padumadasa, Sanjeewa Rajapakse
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) are contraindicated in pregnancy due to fetal toxicity causing neonatal renal failure. However, these can safely be administered during breastfeeding. In women with AF, treatment with beta-blockers and digoxin, and anticoagulation to minimise the risk of thromboembolism, should be considered. In women with heart failure due to pulmonary hypertension, phosphodiesterase type 5 inhibitors such as sildenafil or tadalafil and prostaglandin therapy improve maternal survival. Endothelin receptor antagonists are contraindicated due to teratogenic effects.
Mechanisms of Chemically Induced Glomerular Injury
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Because of its vasoconstrictive properties, endothelin (ET) may play a major role in the control of renal hemodynamics in normal and disease conditions. CSA increases ET synthesis and release either by damaging the endothelium or by directly increasing ET gene expression, possibly in the mesangial cells.6 Cultured human mesangial cells express the gene for ET and secrete the corresponding protein.6 Active production of ET by mesangial cells might contribute to modulate glomerular vascular tone and may thus control glomerular function. Recent studies provide evidence129 that CSA induces a time-and dose-dependent decrease in size of the isolated human glomeruli and a distinct contraction of the cultured mesangial cells (Figure 14). These effects occurred in the absence of renal nervous and extraglomerular humoral influences.129 Therefore, it appears that CSA could trigger mesangial cells to increase synthesis of ET which, in turn, could act in an autocrine mode to stimulate contraction of the mesangial cells themselves, contributing in this way to the alteration of the glomerular function.
Heart disease
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
PAH-targeted therapies should be continued in pregnancy. Specific therapies include: – Phosphodiesterase inhibitors (sildenafil, tadalafil). These can be safely continued or instigated in pregnancy.– Endothelin receptor antagonists (bosentan, ambrisentan). These are usually discontinued in pregnancy, as they are teratogenic in rats.– Prostanoid analogues (epoprostenol – intravenous [i.v.], iloprost – nebulized or i.v.) and nitric oxide – inhaled. These can be safely continued or instituted in pregnancy.
Adjuncts to pulsed dye laser for treatment of port wine stains: a literature review
Published in Journal of Cosmetic and Laser Therapy, 2021
Bing Wang, Xianglin Mei, Yanlong Wang, Xin Hu, Fuqiu Li
Endothelin is a bioactive peptide synthesized by endothelial cells that has vasoconstrictive effect, which is associated with the growth of various tumors. It can inhibit cell apoptosis and promote neovascularization. Endothelin receptor antagonists have been shown to exhibit antiangiogenic effects in animal models (47). Accordingly, some scholars speculated that the endothelin receptor antagonist, bosentan, may inhibit PDL-induced angiogenesis in PWS lesions. Under this assumption, it was used in combination with PDL to treat PWS. Four patients with refractory PWS received bosentan 1 day before the PDL treatment and continued it for 14 days. Three patients showed no or only slight improvement, whereas one patient showed a noticeable improvement at the treated area. At 6-month follow-up, the efficacy was maintained. Subsequently, this patient was continued to be treated, and the lesions also showed blanching. This result indicates that some PWS patients may benefit from systematically administered endothelin receptor antagonists to inhibit angiogenesis after PDL treatment (48).
Endothelial dysfunction: a therapeutic target in bacterial sepsis?
Published in Expert Opinion on Therapeutic Targets, 2021
Jean-Louis Vincent, Can Ince, Peter Pickkers
There are three structurally similar, 21 amino acid isoforms of endothelin (ET-1, −2 and −3), which bind to two endothelin receptors (ETA and ETB). ET-1 is mainly produced by vascular endothelial cells and is a potent vasoconstrictor. An endothelin precursor (big ET-1, or pro-ET-1) consisting of 39 amino acids is cleaved by the endothelin-converting enzyme (ECE), which resides on the endothelial cell membrane, to form ET-1. ET-1 can bind to the ETA receptor on the smooth muscle cells of the vessel wall, leading to vasoconstriction via a cascade of intracellular processes (Figure 4). ET-1 can also bind to the ETB receptor located on the endothelial cell itself. Occupation of the endothelial ETB receptor leads to the production of NO, so that the ETA-induced vasoconstriction is partly reversed. ET-1 production is stimulated by angiotensin II, antidiuretic hormone (ADH), thrombin, cytokines, oxygen radicals, and shear stress on endothelial cells. ET-1 release is also stimulated by endotoxin, which may explain the elevated levels in patients with sepsis [65]. ET-1 release is inhibited by NO, prostacyclin, and atrial natriuretic peptide.
Selexipag for the treatment of pulmonary arterial hypertension
Published in Expert Review of Respiratory Medicine, 2021
Léon Genecand, Julie Wacker, Maurice Beghetti, Frédéric Lador
For the large majority of PAH patients, pulmonary vasoreactivity testing is negative, CCB are not useful and pulmonary vasodilator therapies should be tried. Imbalance between vasoconstrictors (thromboxane, endothelin) and vasodilators (nitric oxide, prostacyclin (PGI2)) is one of the various and complex physiopathological mechanism that leads to the development of PAH. Pulmonary vasodilators target three different pathways: 1) NO, 2) endothelin and 3) PGI2 [6]. NO is a pulmonary vasodilator that can be increased with phosphodiesterase-5 (PDE-5) inhibitors (sildenafil, tadalafil, and verdenafil) or guanylate cyclase stimulators (GCs) (riociguat). Endothelin is a pulmonary vasoconstrictor with mitogenic effects. Endothelin antagonists (bosentan, ambrisentan, macitentan) inhibit endogenous endothelin’s effects resulting in pulmonary vasodilatation. PGI2 have vasodilator, antiplatelet, and antiproliferative properties [7]. Synthetic PGI2 (Intravenous (IV) epoprostenol), PGI2 analogs (beraprost, iloprost, treprostinil), and PGI2 receptor agonist (selexipag) mimic the action of endogenous PGI2.