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Aim To determine whether AngⅡin para-ventricular nucleus (PVN)was involved in the chronic intermittent hypoxia (CIH ) induced-hypertension in rats.Methods Male Sprague-Dawley rats were ran-domly divided into Sham and CIH groups,the Sham rats were exposed to continuous normoxia,while the CIH rats were submitted to CIH (8 h per day for 15 days).The conscious noninvasive method with tail cuff was performed in rats to record the systolic blood pres-sure during establishing the model of CIH induced hy-pertension.Mean arterial pressure (MAP)and heart rate (HR)were recorded in vivo on a PowerLab data acquisition system after CIH.Rats were fixed on the stereotaxic instrument to conduct microinjection in the PVN.We used Western blot to measure Ang Ⅱ level and AngⅡtype 1 receptor (AT1 R)protein expression in PVN.Results The level of PVN Ang Ⅱin CIH rats was significantly higher than that in Sham rats,a-long with increased AT1 R protein expression.Microin-jection of Ang Ⅱ(0.03,0.3,3 nmol)in bilateral PVN dose-dependently increased MAP in both CIH and Sham rats,and this response was significantly augmen-ted in CIH rats.Losartan (50 nmol),AT1 R antago-nist,had no effect on MAP in Sham rats,but caused significant MAP decreases in CIH rats,and prevented Ang Ⅱ-induced increases in MAP in both CIH and Sham rats.Conclusion The results suggest that the increased AngⅡrelease and enhanced AT1 R activation in the PVN contribute to CIH induced-hypertension in rats.
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Besides cyclooxygenase and nitric oxide synthase, another distinct endothelial pathway, endothelium-dependent hyperpolarization factor (EDHF), is involved in relaxation of the vascular smooth muscle cells. EDHF has been demonstrated unequivocally in various blood vessels from different species, including human, and is likely to play an important role in cardiovascular physiology and pharmacology.
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AIM:To study the effects of Hydrogen Peroxide(H2O2)and 11,12-epoxyeicosatrienoic acid(11,12-EET)on EDHF-mediated relaxation in the rat basilar arteries.METHODS: The relaxant effects of acetylcholine(ACh),H2O2,11,12-EET,and catalase(CAT) on rat arteria basilaris in vitro were detected by vasomotoricity experiment in vitro.RESULTS: In the rat basilar arteries,preconstricted by 30 mmol/L KCl in vitro,ACh(10-7-10-4.5 mol/L) had the concentration-dependent relaxation effect.3?10-5 mol/L N?-nitro-L-arginine-methyl-ester(L-NAME) and 10-5 mol/L indomethacin(Indo) could partly inhibit the relaxation effect of ACh to the rat basilar arteries,but non-No/non-PGI2-mediated relaxation was still significant(P
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Objective To study the protective effect of total flavone from Rhododendron simsii(TFRS) on myocardial ischemia-reperfusion injury rats and its mechanism.Methods The ischemic model was made by occluding the anterior descending of the left artery(LAD) in rats.The change of ST segment and T wave of electrocardiograph(ECG) were observed,and the activity of lactate dehydrogenase(LDH),creatine kinase(CK),levels of the maleic dialdehyde(MDA),and nitric oxide(NO) in serum were measured.And by tetrazolium chloride(TTC) staining,the areas of myocardial infarction were observed.The expression of inducible nitricoxide synthase(iNOS) in rats was detected by emploring the reverse transcription-polymerase chain reaction(RT-PCR) technique.Results On the myocardial infarction model by occluding the anterior descending of the LAD in rats,TFRS(100 mg/kg) obviously reduced the height of ST segment after occluding 30 min and TFRS(25,50,and 100 mg/kg) obviously reduced the height of ST segment after reperfusion 30 min.TFRS(50 mg/kg) reduced by myocardial infarction area.TFRS(50 and 100 mg/kg) obviously reduced the activity of CK and LDH.TFRS(50 mg/kg) decreased the level of MDA in serum.By RT-PCR technique,it was found that the expression of iNOS mRNA in myocardium in IR rats pretreated with TFRS(100 mg/kg) was higher than that in IR and normal groups.Conclusions TFRS has the significant protection against myocardial ischemia-reperfusion injury via atte-nuating oxygen free radical and increasing the expression of iNOS mRNA and NO production.
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Aim To study the effect of total flavones of Rhododendra(TFR)on bioelectricity changes of ventricular myocytes in guinea pigs. Methods Conventional microelectrode technique was used to record action potentials (AP) , resting potentials (RP) and effective refractory period (ERP). Results TFR 25,50 mg?L-1 decreased the action potential duration at 50%,90% repolarization (APD50,APD90) while TFR 100,200,400 mg?L-1 prolonged APD50 and APD90Significantlg. TFR 200,400 mg?L-1markedly decreased action potentials amplitude (APA) and velocity maximum of depolarization (Vmax). TFR 400 mg?L-1decreased resting potential. TFR 200 mg?L-1 prolonged ERP. Conclusion TFR may antagonize Ca2+ inward flow at lower concentration and block K+ inward flow at higher concentration.