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Review
. 2000 Sep;131(2):161-8.
doi: 10.1038/sj.bjp.0703570.

5-hydroxytryptamine and the pulmonary circulation: receptors, transporters and relevance to pulmonary arterial hypertension

M R MacLean  1 , P Herve, S Eddahibi, S Adnot
Affiliations
Free PMC article
Review

5-hydroxytryptamine and the pulmonary circulation: receptors, transporters and relevance to pulmonary arterial hypertension

M R MacLean et al. Br J Pharmacol. 2000 Sep.
Free PMC article
No abstract available

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Figures

Figure 1
Figure 1
Diagrammatic representation of the pulmonary arteries within the lung. (A) In the normal lung there is an uneven distribution of smooth muscle phenotypes and numerous non-muscular precapillary vessels (see Figure 2). (B) In the pulmonary hypertensive lung there is progression of muscularization into the non-muscular terminal portion of the arterial tree. This is due to hyperplasia and redistribution of smooth muscle cell phenotypes (see text and Figure 2 for details).
Figure 2
Figure 2
Remodelling of precapillary pulmonary arterioles (PAs) in rat lung following development of pulmonary hypertension. (A) Normal rat lung. Note absence of medial layer. (B) In rats exposed to 2 weeks of hypobaric hypoxia with associated pulmonary hypertension. *Note two elastic laminae separated by distinct medial layer.
Figure 3
Figure 3
The 5-HT Hypothesis of pulmonary arterial hypertension. (A) Platelet handling of 5-HT. 5-HT uptake by platelets through the 5-HTT may be compromised after anorexigen intake, in primary and secondary pulmonary arterial hypertension, in chronic obstructive lung disease and in the fawn-hooded rat which is genetically pre-disposed to pulmonary arterial hypertension. Release of platelet 5-HT may be enhanced by certain anorexigens. This, and perhaps increased accumulation of platelets in the lung, would lead to increased exposure of pulmonary vascular smooth muscle cells to 5-HT. (B) 5-HT and human pulmonary vascular smooth muscle cells. 5-HT can cause pulmonary vascular smooth muscle cell contraction and proliferation. Proliferation occurs through 5-HT uptake by the 5-HTT and subsequent stimulation of superoxide anions and increased tyrosine phosphorylation of GTPase-activating protein. Increased 5-HT exposure combined with increased 5-HTT would potentiate these effects. Increased 5-HTT activity may be secondary to increased 5-HTT transcription stimulated by anorexigens, hypoxia (via HIF-1 activation) and in PPH and secondary PAH. Contraction occurs through 5-HT1B receptor (Gi-coupled) activation which can be enhanced by decreased cyclic GMP levels and through synergy with Gq-coupled receptor activation.
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