Li-Hong Fan

Downregulation of Kir6.1/SUR2B channels in the obese rat aorta.

OBJECTIVE This study was designed to evaluate the contribution of adenosine triphosphate-dependent potassium channels to the increase in blood pressure observed in obese rats. METHODS The experiment was performed in male Sprague-Dawley rats. Glibenclamide-sensitive currents were measured in vascular smooth muscle cells by patch-clamp. Expressions of Kir6.1 and SUR2B were examined by reverse transcription polymerase chain reaction and western blot techniques, respectively. RESULTS In the aortic vascular smooth muscle cells, pinacidil induced glibenclamide-sensitive currents. The current from obese rats was significantly lower (-10.55 +/- 1.63 pA/pF) compared with that from the control rats (-20.18 +/- 2.79 pA/pF). Expressions of Kir6.1 and SUR2B were downregulated in vascular smooth muscle cells of aortas from the obese rats. CONCLUSION These findings suggest that the adenosine triphosphate-dependent potassium channel is downregulated in smooth muscle cells from the aortas of obese rats, which may contribute to the increase in blood pressure in these rats.

High-fat diet may impair KATP channels in vascular smooth muscle cells

K(ATP) channel in vascular smooth muscle cell (VSMC) is closely linked to the etiology of hypertension. The aim of this study was to investigate effect of the high-fat diet-induced obesity on K(ATP) channel and blood pressure. Obesity was induced by a 24-week high-fat diet feeding in rats. Function and expression of K(ATP) channel in mesenteric arteries were examined using myography system, patch clamp and Western blotting. We show that high-fat diet increased blood pressure, decreased K(ATP) channel-mediated relaxation responses and currents, and down-regulated K(ATP) expression in VSMC. In conclusion, diet-induced obesity impairs K(ATP) channels in VSMC, which may underscore obesity-triggered increase in blood pressure.

Effect of PGE2 on DA tone by EP4 modulating Kv channels with different oxygen tension between preterm and term

OBJECTIVE To investigate common downstream mechanism of PGE2 and O2-sensitive voltage-dependent potassium (Kv) channels in preterm and term DA tone regulations, for suggesting respective prescriptions for preterm and term PDA. STUDY DESIGN The expressions of Kv1.2, 1.5 and 2.1 were compared between preterm and term in rabbit and human DAs at mRNA and protein levels; DA contracting responses caused by O2, Kv channels blocker 4-AP, EP4 antagonist GW627368X, and PGE2 reduce using vessels rings and Whole-Cell Patch-Clamp were explored. RESULTS Kv 1.2 and 2.1 expressions were developed with pregnant age in preterm DA and decreased after birth with oxygen stimulation in term DA. GW627368X led significant DA constriction and DASMC IK current decrease in preterm, which was slimier to 4-AP effects, but just slightly influenced on DA tension and DASMC IK current at term. In addition, PGE2 led great DA dilation and IK current increase of DASMC in preterm but not in term. These DA tension and IK current changes were in line with Kv channel expressions. CONCLUSION Higher levels of PGE2 binds with GPCR EP4, which activates G-protein to couple with O2-sensitive Kv channels and to open them, leading to DA vasorelaxation in the fetus. It indicates that EP4 inhibitors, instead of PGE2 or its analogue PGE1, may be a selectable strategy for preterm PDA.

Altered ATP-sensitive potassium channels may underscore obesity-triggered increase in blood pressure.

AbstractAim:To determine whether ATP-sensitive potassium channels are altered in VSMC from arotas and mesenteric arteries of obese rat, and their association with obesity-triggered increase in blood pressure.Methods:Obesity was induced by 24 weeks of high-fat diet feeding in male Sprague-Dawley rats. Control rats were fed with standard laboratory rat chow. Blood pressure and body weight of these rats were measured every 4 weeks. At the end of 24 weeks, KATP channel-mediated relaxation responses in the aortas and mesenteric arteries, KATP channel current, and gene expression were examined, respectively.Results:Blood pressure and body weight were increased in rats fed with high-fat diet. KATP channel-mediated relaxation responses, currents, and KATP expression in VSMC of both aortas and mesenteric arteries were inhibited in these rats.Conclusion:Altered ATP-sensitive potassium channels in obese rats may underscore obesity-triggered increase in blood pressure.

Resistin may be an independent predictor of subclinical atherosclerosis formale smokers

Abstract To investigate whether resistin is associated with early atherosclerosis in male smokers. The present study consecutively enrolled 50 male smokers. Their serum resistin contents were detected with enzyme linked immunosorbent assay (ELISA), and subclinical atherosclerosis indices, including carotid inner middle thickness (IMT) and arterial elasticity indices (C1 and C2), were measured. The association between serum resistin levels and IMT, C1 and C2 were respectively evaluated with the Pearson’s correlation coefficient method. The results showed that the serum resistin level had a positive association with IMT (r = 0.307, p = .030), but were both inversely associated with C1 (r = −0.440, p = .001) and C2 (r = −0.381, p = .006). These associations remained significant even after adjustment for cardiovascular confounders. In conclusion, serum resistin concentration was independently associated with early atherosclerosis in male smokers.

Voltage-Gated Potassium+ Channel Expression in Coronary Artery Smooth Muscle Cells of SHR and WKY

This study aims to compare the expression of genes and the molecular characteristic of voltage-gated K+ channels, which make great effort in maintaining and controlling smooth muscle contraction, cellular membrane potential, and intracellular calcium ion currents in artery smooth muscle cells of SHR and WKY. Expression of potassium ions family in coronary artery was detected through reverse transcription polymerase chain reaction quantitatively. Significant levels of voltage-gated K+ channels α1.2, α1.5, and β1.1 expression were all proved to be significantly higher in smooth muscles of SHR than WKY. Whole-cell voltage-gated K+ channel currents were larger in SHR artery smooth muscles than the ones of WKY. Moreover, the voltage dependence of voltage-gated potassium channel activation was more negative in artery smooth muscle of SHR than that of WKY, while voltage dependence of availability was not different. The above diversity of voltage-gated potassium channel detected in gene expression and electrical character in coronary artery smooth muscle of SHR than that of WKY might be an underling mechanism associated with the membrane potential depolarization in artery smooth muscle of SHR.