Pulmonary hypertension and the serotonin hypothesis: where are we now?

MacLean, M. (2007) Pulmonary hypertension and the serotonin hypothesis: where are we now? International Journal of Clinical Practice, 61(S156), pp. 27-31. (doi: 10.1111/j.1742-1241.2007.01497.x)

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Abstract

In the 1960s, serotonin (5HT) was associated with pulmonary arterial hypertension (PAH) caused by certain diet pills, but has recently been the subject of renewed interest in the field of PAH. Serotonin can be synthesised in the pulmonary endothelium with the rate-limiting step being the activity of tryptophan hydroxylase1 (Tph1). The serotonin is released and can then: (i) pass into the underlying pulmonary smooth muscle cells through the serotonin transporter (SERT) to initiate proliferation and/or (ii) activate serotonin receptors on pulmonary smooth muscle cells to evoke proliferation and/or contraction. Serotonin may also mediate pulmonary fibroblast proliferation via the SERT and/or serotonin receptors. Here we will unravel, discuss and update the `serotonin hypothesis' of PAH in light of recent advances in the field. In conclusion, the activity of serotonin receptors, the SERT and Tph1 can all be elevated in clinical and experimental PAH and each offers a potentially unique therapeutic target.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:MacLean, Professor Margaret
Authors: MacLean, M.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:International Journal of Clinical Practice
ISSN:1368-5031
ISSN (Online):1742-1241

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