Referenced in: none

Automatically associated channels: Cav1.2 , Cav1.3 , Kir6.1 , Kir6.2 , Slo1

Title: Effects of gaseous sulfur dioxide and its derivatives on the expression of KATP, BKCa and L-Ca(2+) channels in rat aortas in vitro.

Authors: Quanxi Zhang, Jingjing Tian, Yunlong Bai, Xiaodong Lei, Mei Li, Zhenhua Yang, Ziqiang Meng

Journal, date & volume: Eur. J. Pharmacol., 2014 Nov 5 , 742, 31-41

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25192964

Abstract
Epidemiological investigations have revealed that sulfur dioxide (SO2) exposure is linked to cardiovascular diseases. Our previous study indicated that the vasorelaxant effect of SO2 might be partly related to ATP-sensitive K(+) (KATP), big-conductance Ca(2+)-activated K(+) (BKCa) and L-type calcium (L-Ca(2+)) channels. The present study was designed to further investigate the effects of gaseous SO2 and its derivatives on the gene and protein expression of these channels in the rat aortas in vitro. The results showed that the mRNA and protein levels of the KATP channel subunits Kir6.1, Kir6.2 and SUR2B of the rat aortas in SO2 and its derivatives groups were higher than those in control group. Similarly, the expression of the BKCa channel subunits α and β1 was increased by SO2 and its derivatives. However, SO2 and its derivatives at 1500μM significantly decreased the expression of the L-Ca(2+) channel subunits Cav1.2 and Cav1.3. Histological examination of the rat aorta tissues showed moderate injury of tunica media induced by SO2 and its derivatives at 1500μM. These results suggest that SO2 and its derivatives can activate the KATP and BKCa channels by increasing the expression of Kir6.1, Kir6.2, SUR2B and α, β1, respectively, while also inhibiting the L-Ca(2+) channels by decreasing the expression of Cav1.2 and Cav1.3 of the rat aortas. The molecular mechanism of the vasorelaxant effect of SO2 and its derivatives might be related to the expression changes of KATP, BKCa and L-Ca(2+) channel subunits, which may play a role in the pathogenesis of SO2-associated cardiovascular diseases.