Teoria serotoninowa a tętnicze nadciśnienie płucne

Monika Kloza 1, Marta Baranowska-Kuczko 2, Anna Pędzińska-Betiuk 1, Konrad Jackowski 1, Hanna Kozłowska 1
1 - Zakład Fizjologii i Patofizjologii Doświadczalnej Uniwersytetu Medycznego w Białymstoku
2 - Zakład Fizjologii i Patofizjologii Doświadczalnej Uniwersytetu Medycznego w Białymstoku; Zakład Farmacji Klinicznej Uniwersytetu Medycznego w Białymstoku
Postepy Hig Med Dosw
2014; 68 738-748
ICID: 1107860
Article type: Review article
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 and
Rho-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 functional
interaction between 5-HT1B receptor and SERT in modulation of vasoconstriction and
proliferation in pulmonary arteries. This review discusses the role of 5-HT in the development
of PAH and highlights possible therapeutic targets within serotonergic system.
DOI: 10.5604/17322693.1107860
PMID 24934532 - kliknij tu by zobaczyć artykuł w bazie danych PubMed

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