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. Author manuscript; available in PMC: 2011 May 11.
Published in final edited form as: Circulation. 2010 May 11;121(18):2045–2066. doi: 10.1161/CIRCULATIONAHA.108.847707

Figure 4. Serotonin (5-HT) abnormalities in PAH.

Figure 4

Increased bioavailability of serotonin during progression of PAH results from an increased release of serotonin from platelets and from an increased synthesis of serotonin by endothelial cells which produce serotonin and express tryptophan hydroxylase-1 (TPH1), the key enzyme controling 5-HT synthesis. Overexpression of 5-HTT (SERT) by PASMC is responsible for the increased mitogenic effect of serotonin on these cells. 5-HT receptors, including 5-HT1B/1D and 5-HT2A receptors mediate 5-HT-induced PA contraction of pulmonary vessels. 5-HT2A receptors located on platelets potentiate the aggregation response to various platelet activators. 5-HT2B receptors expressed by PASMC are also involved in the pulmonary vascular remodeling process.

Figure and legend contributed by Dr. Serge Adnot, Département de Physiologie, Hôpital Henri Mondor, CRETEIL, FRANCE