Serotonin receptors take the TRiPV4 highway in chronic hypoxic pulmonary hypertension. Focus on "TRPV4 channel contributes to serotonin-induced pulmonary vasoconstriction and the enhanced vascular reactivity in chronic hypoxic pulmonary hypertension".

PULMONARY ARTERIAL HYPERTENSION (PAH) is a rare human disease displaying a very poor prognosis of survival. The chronic increase in pulmonary vascular resistance associated with PAH eventually leads to right ventricular hypertrophy and failure, and ultimately death. It is well accepted that the increase in pulmonary arterial resistance to blood flow in PAH primarily involves a partial or complete occlusion of small resistance vessels. Arterial occlusion in PAH is the combined product of increased smooth muscle contractility and enhanced sensitivity to vasoconstrictors, reduction in lumen diameter produced by arterial wall thickening, and increased thrombosis. We still have a poor understanding of the etiology of PAH (1).