Plasma endothelin-1 and -3 in cirrhosis: relationship with systemic hemodynamics, renal function and neurohumoral systems
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Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide y
2013, Journal of HepatologyCitation Excerpt :Furthermore, dysbalanced SNS neurotransmitter release is in accordance with evidence of differential modulation of NA and NPY release in the rat mesenteric bed: endothelins (ET-1, ET-3) have been shown to inhibit NPY release but not NA release [33], closely resembling our results. Considering cirrhosis, circulating plasma levels of endothelin-1 and -3 are elevated [34,35] and therefore could contribute to selective inhibition of NPY release. Finally, the observed accelerated decline of PNS-induced NA release and dysregulated NA release in cirrhosis may reflect reduced expression of genes regulating axonal transport, vesicle trafficking, and exocytosis of catecholamines [11].
Portopulmonary hypertension: From diagnosis to treatment
2011, European Journal of Internal MedicineCitation Excerpt :In addition, the presence of portosystemic shunts allows different vascular mediators to bypass liver metabolism creating an imbalance between vasoconstrictor and vasodilator factors at the level of pulmonary vasculature. Mediators such as endothelin-1, thromboxane A2, Vasoactive Intestinal Peptide (VIP), and serotonin can have direct vasoacitve and mitogenic effects and can cause damage to the pulmonary endothelium [6,19]. The imbalance is further augmented by a decrease in synthesis of vasodilators factors such as nitric oxide (NO) and prostacycline [20,21].
Portopulmonary hypertension and serum endothelin levels in hospitalized patients with Cirrhosis
2011, Hepatobiliary and Pancreatic Diseases InternationalPortopulmonary hypertension: State of the art
2008, Annals of HepatologyCitation Excerpt :A proposed mechanism for POPH includes the increased blood flow (high cardiac output) in chronic liver disease causing vascular wall shear stress, which can activate a cascade of events that may eventually lead to the characteristic vasculopathic changes in POPH, and that also could be present in any form of PAH.13 Increased levels of endothelin-1 (ET-1), a potent vasoconstrictor produced by the pulmonary vascular endothelium and the liver, has been shown to play a role in the pathogenesis of idiopathic PAH, as well as in other forms of PAH.14,15 The presence of portosystemic shunts may allow the shunting of the vasoactive substances from the splachnic circulation to the pulmonary circulation, allowing these vasoactive mediators to bypass the liver metabolism and causing substantial effects in the pulmonary vasculature.2-4
HEPATIC CIRRHOSIS
2008, Pharmacology and Therapeutics: Principles to Practice