Platelet-derived growth factor receptor-β in myocyte was upregulated by angiotensin Ⅱ

To observe the regulation of platelet-derived growth factor (PDGF) receptor-βin myocyte stimulated by angiotensin II (AngII) at both integrated and cellular levels and reveal the signal transduction mechanism in cell, two kidneys, one clip (2K1C) renal hypertension were performed by placing a sliver clip around the left renal artery. Blood pressure and the ratio of left ventricular weight to body weight were measured at 4 and 8 weeks after operation. The content of AngII in heart was detected by radioimmunology assay; the protein level of PDGF receptor-βin heart was measured by Western blot analysis. The alteration of PDGF receptor-βstimulated by AngII and several inhibitors was observed on cultured neonatal rat ventricular myocyte (NRVM). The content of AngII in heart of 2K1C renal hypertensive rat at 4 and 8 weeks after operation was increased. Compared with sham group, 4 and 8 weeks after operation, PDGF receptor-βin heart of 2K1C group was upregulated by 100.3% and 127.1% (P < 0.05), respectively. This upregulation could be inhibited by captopril. For cultured myocyte, PDGF receptor-βwas increased by 47.1% after being stimulated by AngII and this upregulation could be inhibited by losartan which was an inhibitor of AT1 receptor. PLC inhibitor (U73122) and MEK inhibitor (PD98059) could partly inhibit PDGF receptor-βupregulation induced by AngII. These results suggested that AngII could upregulate PDGF receptor-βin myocyte by its AT1 receptor and this effect was at least partly dependent on PLC and extracellular signal-regulated kinase (ERK).     

β-Adrenergic activation enhances NMDA-induced current in pyramidal cells of the basolateral nucleus of amygdala

NMDA receptor （NMDA-R） in the amygdala complex is critical for both long-term potentiation （LTP） and formation of conditioned fear memory. It is reported that activation of β-adrenoceptors （β-AR） in the amygdala facilitates LTP and enhances memory consolidation. The present study examined the regulatory effect of β-AR activation on NMDA-R mediated current in pyramidal cells of the basolateral nucleus of amygdala （BLA）, using whole-cell recording technique. Bath application of the β-AR agonist isoproterenol enhanced NMDA-induced current, and this facilitatory effect was blocked by co-administered propranolol, a β-AR antagonist. The facilitatory effect of isoproterenol on NMDA-induced current could not be induced when the protein kinase A （PKA） inhibitor Rp-cAMPs was added in electrode internal solution.The present results suggest that β-AR activation in the BLA could modulate NMDA-R activity directly and positively, probably via PKA.     

Background current affects the internal wave structure of the northern South China Sea

The internal wave modal equations are solved with the consideration of background currents. Analytical and numerical solutions of some specific examples, including observations in the northern South China Sea （SCS）, are obtained to investigate the effect of back- ground current on internal wave vertical structure. The effects of current shear and curvature on internal wave vertical structure are eval- uated separately. It is found that the phase speed and wave structure are modified by background currents, the current shear has little effect on wave structure, whilst the current curvature could have a strong impact on the wave structure. The extent of the effect by the current curvature on the wave structure depends on the magnitudes of current curvature, relative wave speed, and buoyancy frequency, sometimes the effect by the current curvature may even cause the wave to attenuate severely with depth. A new method to obtain the real eigenfunction with depth in the case that the waves become evanescent is also put forward. It is shown that the residual tidal current in the northern SCS is strong enough to cause the wave to attenuate severely at the uooer laver.     

Population dynamics and spatial distribution of microbial species in multispecies biofilms under the action of direct electric current

The metabolism, population dynamics and spatial distribution of nitrifying bacteria and heterotrophs in biofilms under the action of direct electric current were investigated by using the micro-slicing technique. The nitrification rate of nitrifying bacteria was severely inhibited by a current over 10 Am^-2 at lower C/N ratios. Compared to heterotrophs, the nitrifying bacteria in the surface biofilms were severely inhibited, resulting in a significant decrease in bacterial density. An increase in current density narrowed the less current-sensitive inner biofilm region, and in addition the density of NO2-oxidizers decreased more significantly than that of NH4-oxidizers in the surface biofilms probably due to electrochemical reactions at the anode. However, the effect of current on both the population dynamics and the spatial distribution of the microbial species was less significant at larger C/N ratios.     

Investigation of the deterioration of passive films in H_2S-containing solutions

The effect of H_2S on the corrosion behavior of 316 L stainless steel was investigated using electrochemical methods by changing the gas condition from CO_2 to H_2S and then back to CO_2. The presence of H_2S showed an acceleration effect on the corrosion of 316 L stainless steel in comparison with CO_2. The acceleration effect remained even after the complete removal of H_2S by CO_2, indicating that the passive film was irreversibly damaged. X-ray photoelectron spectroscopy(XPS) analysis indicated that the passive film was composed of Cr_2O_3, Fe_2O_3, and FeS_2 after being immersed in H_2S-containing solutions. The semiconducting property of the passive film was then investigated by using the Mott–Schottky approach. The presence of sulfides resulted in higher acceptor and donor densities and thus was responsible for the deterioration of passive films.     

Effects of niacin on nitric oxide synthase expression in rat lungs exposed to silica

The aim of this study was to evaluate the effects of niacin in diet on the expression of nitric oxide synthase (NOS) in rat lungs of the animal model of silicosis established by direct tracheal instillation of silica particles into rat lungs surgically. The niacin concentration in serum was analyzed by high performance liquid chromatography (HPLC). The expression of inducible nitric oxide synthase (iNOS) protein in paraffin-embedded lung sections was determined by streptavidin/peroxidase (SP) staining. Quantitative analysis by Image-Pro Plus was also performed on the expression of iNOS. The results showed that niacin concentration in serum of the niacin-treated rats was significantly higher than that in the control and silica-treated rats. After 7 days of silica instillation, iNOS integrated optical density (IOD) in rat lungs and total NOS and iNOS activities in bronchoalveolar lavage fluid (BALF) in silica-treated rats rose by 273420.75, 2.61 units/mL and 1.89 units/mL respectively, when compared with those in the control rats. Niacin treatment significantly reduced silica-induced iNOS IOD in rat lung tissues and total NOS and iNOS activities in BALF supernatant by 248292.35, 1.50 units/mL and 0.91 units/mL, respectively, as compared with those in silica-treated rats. Therefore, niacin can effectively attenuate the pathological expression of NOS in rat lung tissues induced by silica particles.     

Corrosion behavior of Ni–P/nano-TiC composite coating prepared in electroless baths containing different types of surfactant

In current research, in order to enhance the incorporation of nano-sized TiC particles into electroless Ni–P (EN) coating, different types of surfactant (cationic, anionic, and polymeric) were added to the plating bath. The effects of addition of the surfactants on surface morphology, deposition rate, TiC and P contents of the prepared coatings were investigated. The surface morphology was evaluated by scanning electron microscopy (SEM). It was demonstrated that in the presence of the anionic, polymeric and somehow cationic surfactants, TiC nano-particles were embedded in the matrix which influenced the surface morphology. The effect of surfactant types on the corrosion properties of Ni–P/TiC coated steel was also studied. Corrosion behavior of the coated steel was evaluated by potentiodynamic polarization and electrochemical impedance spectroscopy (EIS) which affected by the incorporation of TiC particles into the Ni–P matrix. The level of corrosion resistance improvement depended largely on the phosphorous and TiC concentration of the applied coating.     

Regulation of angiotensinⅡon Gaq/11 protein of vascular smooth muscle cell and its underlying mechanism

To study the regulation of angiotensin Ⅱ(Ang Ⅱ) on Gαq/11 protein of vascular smooth muscle cell (VSMC) and its underlying mechanism, the protein synthesis was detected by [3H]-leucine incorporation. G?q/11 expression was measured by Western blot in cultured VSMC of rat aorta. The results showed that the level of G?q/11 was downregulated after stimulated by AngⅡ for 1-6 h, while it was upregulated significantly by 12-24 h stimulation (P < 0.01) in VSMC. The [3H]-leucine incorporation of VSMC was increased after 24 h Ang Ⅱ stimulation. The biphase regulation of Ang Ⅱ on G?q/11 protein was blocked by the Ang Ⅱ type Ⅰ receptor (AT1) specific antagnist losartan or PLC inhibitor U73122, while PD98059 did not have this effect. These data indicated that Ang Ⅱ contributed to VSMC hypertrophy by regulating the level of G?q/11, and this effect was mediated mainly through AT1 receptor-PLC signal transduction pathway.     

Effect of current density on the morphology of Zn electrodeposits

The effect of current density on the morphology of Zn electrodeposits prepared by a flow-channel cell was investigated by scanning electron microscopy (SEM). It was found that the morphology of Zn electrodeposits evolves from thin-layered hexagonal η-phase crystals to pyramidal η-phase particles with increasing the current density. The morphological evolution at various flow rates was also examined and the results show that the morphological evolution at a lower flow rate is more remarkable than that at a higher flow rate with increasing the current density. To reveal the mechanism of the morphological evolution in detail, the atomic configuration on both (0001)_η and {1100}_η planes under different current densities was investigated, it was noted that a specify current density could provide a good condition for the layered epitaxial growth of hexagonal η-phase.     

Effect of ytterbium on sodium current and its kinetics in rat hippocampal neurons

This study addressed the effects of Yb3＋ on voltage-gated sodium currents in rat hippocampal neurons using the whole-cell patch-clamp technique. Voltage-clamp recordings in single neurons were filtered and stored in a computer. Yb3＋ increased the amplitude of sodium currents in a concentration-dependent and voltage-dependent man- ner. The 50 % enhancement concentration of Yb3＋ on sodium currents was about 8.97 μmol/L, which was dif- ferent from the inhibitory effects of Yb3＋ on potassium current. The analysis on the activation and inactivation kinetics of Na＋ current showed that 100 μmol/L Yb3＋ did not change the process of activation and inactivation. In addition, the times reaching the peak of current （t） and inactivated time constant （τ） were voltage dependent. 100 μmol/L Yb3＋ significantly prolonged the time to peak at -70 and -80 mV. The effect disappeared at the positive direction of -70 mV. Furthermore, Yb3＋ decreased r val- ues to more positive values than -80 mV. In total, Yb3＋ did not change the process of activation, but impelled inacti- vated process. Yb3＋ mainly increased the Na＋ current through changing its conductance. It might be one of the mechanisms that Yb3＋ affected the hippocampal neurons.     

Study of transmembrane La3+ movement in rat ventricular myocytes by the patch-clamp technique

We have studied transmembrane La3+ movement in rat ventricular myocytes for the first time by using the whole-cell patch-clamp recording mode. La3+ (0.01-5.0 mmol/L) could not bring out inward currents through the L-type calcium channel in rat ventricular myocytes, while it could enter the cells by the same way carried by 1μmol/L ionomycin. When the outward Na+ concentration gradient is formed, La3+ can enter the cells via Na-Ca exchange, and the exchange currentsincrease with the increase of external La3+ concentrations. But compared with Na-Ca exchange currents in the same concentration, the former is only 14%-38% of the latter. The patch-clamp experiment indicates that La3+ normally can not enter ventricular myocytes through L-type calcium channel, but it can enter the cells via Na-Ca exchange.     

碘化N-正丁基氟哌啶醇对大鼠缺氧复氧心肌细胞钠钙交换体电流的抑制作用

碘化N-正丁基氟哌啶醇(N-n-butyl haloperidol iodide,F2)为本研究室改造合成的新化合物。前期研究发现F2作为L-型钙通道拮抗剂,能剂量依赖地拮抗缺血再灌注所导致的大鼠心脏损伤。研究F2对缺氧复氧(hypoxia/reoxygenation,H/R)大鼠心肌细胞钠钙交换体电流的作用并探讨其保护机制。采用Langendorff灌流系统灌流SD大鼠心脏,标准酶解法消化分离得到单个心室肌细胞。正常台式液灌流5min,立即灌流充90%N2-10%CO2的缺氧液,建立体外心肌细胞H/R模型,采用全细胞膜片钳技术记录对照、模型以及不同浓度F2(0.1、1、10μmol/L)对心肌细胞钠钙交换体电流,观察H/R状态F2对心肌细胞钠钙交换体电流的影响。结果显示:缺氧抑制钠钙交换体电流主要是抑制外向电流;H/R引起钠钙交换体电流增大,尤其是外向电流的增大。F2呈浓度依赖地抑制钠钙交换体电流,钠钙交换体电流I-V曲线上移。以上表明:F2能抑制钠钙交换体电流,尤其是外向电流,防止H/R时心肌细胞的钙超载,保护心肌细胞。     

Effects of ytterbium on outward K<Superscript>+</Superscript> currents in NIH3T3 cell

Using the whole cell patch-clamp technique, we observed the outward K+ currents and studied for the first time the effects of Yb3+ on the currents and kinetics of activation and inactivation in non-excitable NIH3T3 cell. Our results show that the outward K+ currents were promoted with increasing concentration of Ca2+ in pipette solution and saturated at the concentration of 100 μmol/L Ca2+. Yb3+ in bath solution inhibited the currents in a concentration-dependent manner. At the concentration of 1 μmol/L, Yb...     

Na-Ca exchange current in mammalian heart cells

Electrogenic Na-Ca exchange has been known to act in the cardiac sarcolemma as a major mechanism for extruding Ca ions. Ionic flux measurements in cardiac vesicles have recently suggested that the exchange ratio is probably 3 Na:1 Ca, although a membrane current generated by such a process has not been isolated. Using the intracellular perfusion technique combined with the whole-cell voltage clamp, we were able to load Na+ inside and Ca2+ outside the single ventricular cells of the guinea pig and have succeeded in recording an outward Na-Ca exchange current while blocking most other membrane currents. The current is voltage-dependent, blocked by La3+ and does not develop in the absence of intracellular free Ca2+. This report presents the first direct measurement of the cardiac Na-Ca exchange current, and should facilitate the study of Ca2+ fluxes during cardiac activity, together with various electrical changes attributable to the Na-Ca exchange and the testing of proposed models.     

Voltage dependence of Na/K pump current in isolated heart cells

The Na/K pump usually pumps more Na+ out of the cell than K+ in, and so generates an outward component of membrane current which, in the heart, can be an important modulator of the frequency and shape of the cardiac impulse. Because it is electrogenic, Na/K pump activity ought to be sensitive to membrane potential, and it should decline with hyperpolarization. However, such voltage dependence of outward pump current has yet to be demonstrated, one reason being the technical difficulty of accurately measuring pump current over a sufficiently wide voltage range. The whole-cell patch-clamp technique allows effective control of both intracellular and extracellular solutions as well as membrane voltage. Applying this technique to myocardial cells isolated from guinea pig ventricle, we have measured Na/K pump current between -140 mV and +60 mV, after minimizing passive currents flowing through Ca2+, K+ and Na+ channels. We report here that strongly activated pump current shows marked voltage dependence; it declines steadily from a maximal level near 0 mV, becoming very small at -140 mV. Pump current-voltage relationships will provide essential information for testing models of the Na/K pump mechanism and for predicting pump-mediated changes in the electrical activity of excitable cells.     

La~(3+)掺杂Bi_(0.5)(Na_(1-x-y)K_xLi_y)_(0.5)TiO_3陶瓷的微结构与电学性能

利用传统的电子陶瓷工艺制备了La^3＋掺杂Bi0．5（Na1-x-yKxLiy）0．5TiO3无铅压电陶瓷,研究了La^3＋掺杂对该体系陶瓷的介电压电性能与微观结构的影响．结果表明,少量的La^3＋掺杂可以改善该陶瓷的微结构;当掺杂量为0．1％时,该陶瓷体系的压电性能有较大的改善,室温下该体系配方的压电常数d33可达215pC／N,径向机电耦合系数kp达到37．4％,但同时介电损耗增大,机械品质因子降低．当掺杂量达到1．5％以后,陶瓷的压电性能严重下降．     

Sympathetic regulation of cardiac calcium current is due exclusively to cAMP-dependent phosphorylation.

The positive inotropic effect of the sympathetic nervous system on the heart is partly mediated by an increase in the voltage-gated Ca2+ current (ICa). This increase is generally attributed to beta-adrenergic receptor-stimulated cyclic AMP-dependent phosphorylation of the Ca2+ channel. It has been suggested that cAMP-dependent phosphorylation cannot explain all the effects of beta-adrenergic agonists on ICa and that a parallel membrane-delimited pathway involving the 'direct' action of the G protein Gs also stimulates ICa. A precedent exists for such a membrane-delimited pathway in the activation of a K+ channel by acetylcholine in heart. A membrane-delimited pathway for stimulation of ICa might be important in rapid beat-to-beat regulation of contraction by the sympathetic nervous system, because isoproterenol may produce a biphasic increase in ICa with the rapid phase (tau = 150 ms) putatively mediated by the direct pathway and the slow phase (tau = 35 s) by cAMP-dependent phosphorylation. Here we report that in frog, rat, and guinea pig ventricular myocytes ICa increases slowly and monophasically in response to isoproterenol. The increase is completely blocked by inhibitors of cAMP-dependent phosphorylation. Furthermore, the time course of the increase in ICa closely parallels the increase in contractile force produced by sympathetic nerve stimulation. These data refute earlier suggestions that regulation of Ca2+ channels by the sympathetic nervous system involves or requires a direct G-protein pathway.     

Effects of protein kinase C activators on cardiac Ca2+ channels

Phorbol esters have marked effects on voltage-dependent Ca2+ channels. Inhibitory and stimulatory effects on cardiac Ca2+ channels have been attributed in both cases to activation of protein kinase C. We show that the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate stimulates dihydropyridine-sensitive 45Ca2+ influx in primary cultures of neonatal rat ventricular myocytes within 5 s, but that after a 20-min pre-incubation period the phorbol ester markedly inhibits 45Ca2+ influx. The sequence of stimulation followed by inhibition is confirmed in cell-attached patch clamp recordings of single Ca2+ channel currents. The stimulatory effect is faster at 0 mV than at -40 mV, leading to the novel conclusion that the rate of protein kinase C activation is modulated by the state of the Ca2+ channel.     

Glucagon stimulates the cardiac Ca2+ current by activation of adenylyl cyclase and inhibition of phosphodiesterase

Glucagon exerts positive inotropic and chronotropic effects in the heart. Like its glycogenolytic effect in liver cells, the cardiac effects of glucagon are often correlated with adenylyl cyclase stimulation. Therefore, cyclic AMP-dependent phosphorylation of L-type Ca2+ channels might be involved in the inotropic effect of glucagon. There have been no reports, however, of the effects of glucagon on the cardiac Ca2+ current (ICa). Also, the physiological effects of glucagon could involve mechanisms other than stimulation of adenylyl cyclase. Here we show that glucagon enhances ICa in frog and rat ventricular myocytes. The effect of glucagon in rats resulted from a stimulation of adenylyl cyclase. In frogs, however, the effect of glucagon on ICa was smaller and occurred at a concentration tenfold lower than in rats, and adenylyl cyclase was not modified. In addition, cAMP potentiated the effect of glucagon on ICa in frog ventricle, which correlated with the observed inhibition by glucagon of low-Km cAMP phosphodiesterase activity. Therefore, this is an example of a hormone that affects cardiac function in a similar way to a variety of synthetic cardiotonic compounds, such as milrinone and Ro-20-1724. Inhibition of phosphodiesterase activity by glucagon may be essential in animals in which glucagon increases cardiac contractility but does not effectively stimulate adenylyl cyclase.     

Acetylcholine activation of single muscarinic K+ channels in isolated pacemaker cells of the mammalian heart

Acetylcholine (ACh) released on vagal stimulation reduces the heart rate by increasing K+ conductance of pacemaker cells in the sinoatrial (S-A) node. Fluctuation analysis of ACh-activated currents in pacemaker tissue showed this to be due to opening of a separate class of K+ channels gated by muscarinic ACh receptors (m-AChRs). On the other hand, it has been suggested that m-AChRs may simply regulate the current flow through inward rectifying resting K+ channels (gk1). We report here the measurement of ACh-activated single channel K+ currents and of resting K+ channel currents in isolated cells of the atrioventricular (A-V) and S-A node of rabbit heart. The results show that the ACh-dependent K+ conductance increase in nodal cells is mediated by K+ channels which are different in their gating and conductance properties from the inward rectifying resting K+ channels in atrial and ventricular cells. The resting K+ channels in nodal cells are, however, similar to those activated by ACh.