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Acta Physiol (Oxf). 2013 Jan;207(1):183-93. doi: 10.1111/j.1748-1716.2012.02478.x. Epub 2012 Sep 4.

Secondhand cigarette smoke exposure causes upregulation of cerebrovascular 5-HT(1) (B) receptors via the Raf/ERK/MAPK pathway in rats.

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1
Division of Experimental Vascular Research, Department of Clinical Sciences, Lund University, Lund, Sweden.

Abstract

AIM:

Cigarette smoke exposure increases the risk of stroke. Upregulation of 5-hydroxytryptamine 1B (5-HT(1) (B) ) receptors is associated with the pathogenesis of cerebral ischaemia. This study examined the hypothesis that the expression of 5-HT(1) (B) receptors is altered in brain vessels after secondhand smoke (SHS) exposure.

METHODS:

Rats were exposed to SHS in vivo for 200 min daily for 8 weeks. The contractile responses of isolated cerebral arteries were studies by a sensitive myograph. The mRNA and protein expression for 5-HT(1) (B) receptors were examined by real-time PCR, Western blot and immunofluorescence respectively. In addition, the phosphorylation of Raf/extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinases (MAPK) pathway was evaluated.

RESULTS:

The results showed that SHS exposure shifted the 5-HT(1) (B) receptor-mediated concentration-contraction curve towards the left with a markedly increased maximal contraction. Furthermore, there were significant elevations in mRNA level and protein expression of 5-HT(1) (B) receptors in SHS-exposed rats. Immunostaining revealed that the 5-HT(1) (B) receptors were localized to the smooth muscle cells of cerebral arteries. SHS was also found to induce the phosphorylation of Raf-1 and ERK1/2 proteins. The administration of a Raf-1 inhibitor GW5074 attenuated the 5-HT(1) (B) receptor upregulation.

CONCLUSION:

Secondhand smoke exposure upregulates cerebrovascular 5-HT(1) (B) receptors in rats. The receptor upregulation is associated with Raf/ERK/MAPK activation.

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