Teoria serotoninowa a tętnicze nadciśnienie płucne
Journal Title: Advances in Hygiene and Experimental Medicine - Year 2014, Vol 68, Issue
Abstract
Pulmonary arterial hypertension (PAH) is a progressive, complex disease leading to the right ventricular failure and premature death. PAH is characterized by increased pulmonary arterial pressure, increased vascular resistance, pulmonary vascular remodeling and endothelial dysfunction. Pathomechanism of this disease is still unknown. It has been suggested, that endothelial dysfunction is caused by unbalance between vasodilators and vasoconstrictors e.g. serotonin (5-HT). Previously, serotonin hypothesis was linked to the anorexigens, derivatives of fenfluramine, which are serotonin transporter (SERT) substrates. Nowadays, it has been proved that all elements of serotonergic system within pulmonary circulation participate in the developement of PAH. The tryptophan hydroxylase 1 (Tph-1) catalyses synthesis of 5-HT from tryptophan in the pulmonary arterial endothelial cells. 5-HT mediates contraction of pulmonary vessels via 5-HT1B and 5-HT2A receptors. 5-HT is also transported into pulmonary arterial smooth muscle cells via SERT and through activation of reactive oxygen species andRho-kinase may contribute to contraction or/and, via stimulation of transcription factors,lead to proliferation and remodelling. There is also increasing number of evidence about functionalinteraction between 5-HT1B receptor and SERT in modulation of vasoconstriction andproliferation in pulmonary arteries. This review discusses the role of 5-HT in the developmentof PAH and highlights possible therapeutic targets within serotonergic system.
Authors and Affiliations
Monika Kloza, Marta Baranowska-Kuczko, Anna Pędzińska-Betiuk, Konrad Jackowski, Hanna Kozłowska
Keywords
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