Comparison of agonists-induced contraction between main and the third-order branches of pulmonary arteries in rats / 生理学报

This study was designed to observe the differences between main pulmonary arteries and the third-order branches of pulmonary arteries in the contractile response to phenylephrine (Phen), endothelin-1 (ET-1) and potassium chloride (KCl). The vascular tension changes of main and the third-order branches of pulmonary arteries induced by KCl, ET-1 and Phen were recorded by traditional vascular tone detection methods and microvascular ring technique, respectively. The results showed that Phen could cause a significant contraction in main pulmonary arteries, but did not induce apparent contraction in the third-order branches of pulmonary arteries. Compared with main pulmonary arteries, ET-1 contracted the third-order branches of pulmonary arteries with reduced maximal response value and PDvalue. In comparison with the main pulmonary arteries, contraction caused by KCl was enhanced in the third-order branches of pulmonary arteries. The results suggest that the vascular reactivity of main and the third-order branches of pulmonary arteries is different and it is important to study the vascular function of small branches of pulmonary arteries. This study could provide an important experimental basis for the further study on vascular function of small branches of pulmonary arteries and the functional changes in pulmonary hypertension.

Effects of chronic hypoxia on left and right ventricular function and the expression of cardiac TRPC channels in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the effects of chronic hypoxia on left and right ventricular function and the expression of cardiac transient receptor potential canonical (TRPC) channels in rats.</p><p><b>METHODS</b>Forty eight SD male rats were randomly divided into control group (CON) and chronic hypoxic pulmonary hypertension model group (CH) (n = 24). In CH group, rats were exposed in chronic hypoxia environment (10% +/- 0.2% O2) to induce myocardial hypertrophy. After 3 weeks, mean systemic arterial pressure (mSAP), right ventricular systolic pressure (RVSP), left ventricular systolic pressure (LVSP), left or right ventricular pressure maximum rate of rise (LV/RV + dp/dt(max)), left or right ventricular pressure maximum rate of descent (LV/RV-dp/dt(max)), right ventricular hypertrophy index (RVMI) and left ventricular hypertrophy index (LVMI) were measured. Left and right ventricular myocardium tissue sections were stained by HE and observed under light microscope. Real-time polymerase chain reaction (real-time-PCR) and Western blot were performed to detect the expression of TRPC subfamily.</p><p><b>RESULTS</b>RVSP, RVMI, RV + dp/dt(max) and RV-dp/dt(max) were markedly elevated in CH group (P < 0.01) in comparison to CON group. LVMI was markedly reduced in CH group in comparison to CON group (P < 0.01). LVSP, LV + dp/dt(max) and LV- dp/dt(max) had no significant changes in CH group in comparison to CON group. Right ventricular myocardial cells of CH group became thick, the nuclei stained deeply, the shape of nuclei became not regularity. Left ventricular myocardial fibers did not change significantly. There was significant difference in the levels of mRNA and protein of TRPC1 between CON and CH groups.</p><p><b>CONCLUSION</b>For three weeks exposed to chronic hypoxia induced right ventricular hypertrophy specifically, raised the mRNA and protein expression of TRPC1 on right ventricular myocardial cells . TRPC1 might be involved in the development of cardiac hypertrophy.</p>

TRPC6 mediates the enhancements of pulmonary arterial tone and intracellular Ca2+ concentration of pulmonary arterial smooth muscle cells in pulmonary hypertension rats / 生理学报

Pulmonary arterial hypertension is associated with profound vascular remodeling and alterations in Ca2+ homeostasis in pulmonary arterial smooth muscle cells (PASMCs). Recent studies show that canonical transient receptor potential channel 6 (TRPC6) genes, which encode receptor-operated cation channels (ROCC) in PASMCs, play an important role in Ca2+ regulation and cell proliferation. The aim of the present study was to investigate the role of TRPC6 in monocrotaline (MCT)-induced pulmonary artery hypertension. Sprague-Dawley rats were randomly divided into normal control group and MCT group. In MCT group, pulmonary arterial hypertension was induced by a single intraperitoneal injection of MCT at a dose of 60 mg/kg. After 3 weeks, the right ventricular systolic pressure (RVSP) and the right ventricular mass index (RVMI) were measured. The lung sections were stained by HE and observed under light microscope. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot were performed to detect the expression of TRPC6 in rat pulmonary arteries. The 1-oleoyl-2-acetyl-sn-glycerol (OAG)-induced contractile tension of pulmonary arteries were measured by vascular ring tension analysis and the intracellular Ca2+ concentration ([Ca2+](i))of PASMCs was monitored using Fluo3-AM assay. The results showed that RVSP and RVMI markedly elevated in MCT group (P<0.01) in comparison to CON group. The thickness of pulmonary vascular smooth muscles was increased and the inner diameter of pulmonary arteries was diminished in MCT group. Though there was no significant difference in the levels of mRNA and protein of TRPC6 between CON and MCT groups, the application of OAG, which can directly activate ROCC, induced greater contraction tension of pulmonary arteries (P<0.01) and more Ca2+ entries in PASMCs (P<0.05) in MCT group compared to those in control group. These results indicate that MCT induces pulmonary artery hypertension and thus remodeling of the right ventricle and pulmonary arteries in rats. The expression of mRNA and protein of TRPC6 is not potentiated by MCT, but the TRPC6/ROCC-mediated Ca2+ entry in PASMCs and vascular tone of pulmonary arteries are significantly increased with MCT treatment.