Ning Zhong

University of California, San Francisco, San Francisco, California, United States

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Publications (14)21.66 Total impact

  • Yi Zhang · Ning Zhong · Zhao-Nian Zhou ·
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    ABSTRACT: This study was conducted to investigate the role of the L-type calcium channel in the cardioprotection afforded by chronic intermittent hypobaric hypoxia (CIHH). Rats were exposed to CIHH for 28 days (CIHH28) or 42 days (CIHH42), respectively, before their ventricular myocytes were isolated for electrophysiological studies. Under normal recording conditions, no difference was found in the current density and voltage dependence of activation and inactivation of I(caL) recorded in CIHH28 and CIHH42 myocytes, compared with those in control myocytes isolated from rats exposed to sea-level air. Under simulated ischemic (I) conditions, the peak I(ca.L) decreased in all groups. However, the decreases of I(caL) in CIHH rats were of a lesser extent than those in the control. Simulated ischemia also induced an approximately 10-mV positive shift of the steady-state inactivation curve of I(caL) in control but not in CIHH myocytes, as measured by the half-maximal inactivation potentials (V(1/2)). The results suggest that adaptation to CIHH might have increased the tolerability of cardiac myocytes to ischemic challenges through preventing electrophysiological remodeling of the calcium channel.
    High altitude medicine & biology 04/2010; 11(1):61-7. DOI:10.1089/ham.2009.1011 · 1.28 Impact Factor
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    Fang Yuan · Zan Guo · Ying Xu · Xin Wang · Hui-Min Bu · Ning Zhong · Yi Zhang · Zhao-Nian Zhou ·
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    ABSTRACT: The aim of this study is to investigate the effects of chronic intermittent hypobaric hypoxia (IHH) and chronic continuous hypobaric hypoxia (CHH) on hemodynamics under basic normoxia and acute hypoxia conditions and to find the difference of two types of chronic hypoxia. Forty adult male Sprague-Dawley (SD) rats were randomly divided into 5 groups: Control group (CON), 28 days IHH group (IHH28), 42 days IHH group (IHH42), 28 days CHH group (CHH28) and 42 days CHH group (CHH42). The rats in IHH groups were treated with intermittent hypoxia (11.1% O2) mimicking 5 000 m altitude in a hypobaric chamber for 28 or 42 d, 6 h a day, respectively. The rats in CHH groups lived in the hypobaric chamber with the same degree of hypoxia like IHH rats except half an hour in normoxia each day for feeding and cleaning. The body weight of rats was measured once a week. The parameters in hemodynamics, such as mean artery blood pressure (MAP), heart rate (HR), left ventricular systolic pressure (LVSP), maximum change rate of left ventricular pressure (+/-LVdP/dt(max)) were recorded under basic normoxia and acute hypoxia conditions through catheterization technique. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in myocardium of rats were measured by biochemical method. The weights of whole heart, left and right ventricles were measured separately. The results showed: (1) The basic HR and MAP in CHH42 rats were lower than those in CON, IHH and CHH28 rats (P<0.05). (2) IHH showed a cardioprotection against acute hypoxia and reoxygenation injury, manifested as the result that the changes of HR, MAP, LVSP, and +/- LVdP/dt(max) were smaller than those in CON rats during acute hypoxia and reoxygenation. CHH showed a rather strong cardioprotection during acute hypoxia, manifested as the result that the decreases of HR, MAP, LVSP, and +/- LVdP/dt(max)were much smaller, but it did damage during reoxygenation, manifested as the result that the recovery of hemodynamics was the worst among three groups (P<0.05). (3) The antioxygenation of heart was increased in both IHH and CHH rats compared with that in CON rats manifested by the increased SOD activity and decreased MDA content (P<0.05, P<0.01). (4) IHH had no effect on heart weight, but CHH rats showed an obvious right ventricular hypertrophy compared with CON and IHH animals (P<0.01). The result indicates that IHH can induce a more effective cardioprotection with no much side effect, which might have a potential value for practical use.
    Sheng li xue bao: [Acta physiologica Sinica] 12/2008; 60(6):687-94.
  • Yi Zhang · Ning Zhong · Jiying Gia · Zhaonian Zhou ·
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    ABSTRACT: We examined the effects of chronic intermittent hypoxia (IH) on the hemodynamics of systemic circulation in rat. Chronic IH has no effect on the hemodynamics in the normoxia condition, but it could effectively prevent the fall of hemodynamics during acute hypoxia.
    The Japanese Journal of Physiology 05/2004; 54(2):171-4. DOI:10.2170/jjphysiol.54.171 · 1.04 Impact Factor
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    Qi-zhi Fang · Ning Zhong · Yi Zhang · Zhao-nian Zhou ·
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    ABSTRACT: To characterize the electrophysiological and kinetic properties of Ca2+-activated chloride channel (CaCC) in cultured human umbilical vein endothelial cell line (HUVEC), and test the inhibitory effects of tetrandrine (Tet) on CaCC. Ca2+-activated Cl- currents (I(Cl,Ca)) were recorded by patch-clamp whole cell configurations. [Ca2+]i was measured via intracellular Fura-2 fluorescence intensities. I(Cl,Ca) was activated by increasing [Ca2+]i via direct elevation of intracellular calcium. I(Cl,Ca) showed an apparent outward rectification properties, and it was activated in a voltage- and calcium-dependent mode. Tet dose-dependently inhibited I(Cl,Ca), the IC50 was (5.2+/-0.4) micromol/L (n=8 cells). Tet suppressed both voltage-dependent and calcium-dependent activation of I(Cl,Ca). The activation time constant was (326+/-12) ms [in the presence of 10 micromol/L Tet, compared to control (175+/-17) ms, at +100 mV], and Ca2+ concentration for half maximal activation was (387+/-61) nmol/L for Tet (compared to control (287+/-36) nmol/L. Tet effectively blocked I(Cl,Ca), and such effects might be due to its inhibitory effects on the activation process of Ca2+-activated chloride channel.
    Acta Pharmacologica Sinica 04/2004; 25(3):327-33. · 2.91 Impact Factor
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    ABSTRACT: To study the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxy-phenyl-ethylamino) propane hydro-chloride (DDPH) on the rapidly activating component (I(Kr)), and the slowly activating component (I(Ks)) of the delayed rectifier potassium current (I(K)) in guinea pig ventricular myocytes. Whole-cell patch clamp recording techniques. DDPH (0.1-100 micromol/L) blocked the I(Kr) in a concentration-dependent manner. The IC50 (micromol/L) was 6.1 (95 % confidence limits: 2.8-13.5). IC50 (micromol/L) of DDPH blocking I(Ks) was 12.5 (95 % confidence limits: 4.8-32.2). DDPH (10 micromol/L) did not affect activation time constants and the voltage-dependent activation of both I(Kr) and I(Ks), the half-activation voltage (V1/2, mV) and slope factor (k, mV) were I(Kr): -23.5+/-2.4 and 8.1+/-2.2 [in presence of DDPH, P >0.05, compared with control, V1/2 (-21.7+/-0.8) and k (5.9+/-0.8)]; I(Ks): 27.1+/-0.7 and 16.6+/-0.8 [in presence of DDPH, P >0.05, compared with control, V1/2 (27.0+/-0.8) and k (14.9+/-0.9)]. DDPH slightly increased the deactivation time-constant of I(Kr) ( r) and I(Ks) ( s) at low concentration (<10 micromol/L). The inactivation of I(Kr) was significantly accelerated by DDPH. DDPH inhibited both I(Kr) and I(Ks). The blockade was not due to its influence on activation, but the process of deactivation. The blocking of I(Kr) by DDPH was further associated with its acceleration the channel inactivation.
    Acta Pharmacologica Sinica 07/2002; 23(7):601-8. · 2.91 Impact Factor
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    ABSTRACT: To determine the effects of simulated intermittent high altitude hypoxia adaptation (IHA) on coronary capillary and coronary flow (CF) in rat hearts. Model of Langendorf-perfused isolated rat hearts were used to measure CF during ischemia-reperfusion, and immunoperoxidase staining assay and computer-aid morphometry analysis were conducted to determine the myocardial capillary densities. Cyclic GMP (cGMP) level in myocardium was measured by radio-immunoassay. Pre-ischemia level of CF in IHA rats was higher (IHA28 13.4 mL/min+/-1.5 mL/min, IHA42 15.4 mL/min+/-2.0 mL/min, P < 0.01) than that of normoxic rats (11.0+/-0.8) mL/min, and the recovery of CF after ischemia-reperfusion was better in IHA rats. As an adaptive result, the myocardial capillary densities of the left ventricular myocardium in IHA rats were 1.5 times of those in normoxic control rats, but there was no apparent ventricular hypertrophy in IHA rats. Myocardial cGMP content (1.8+/-0.7) nmol/g in IHA rats were increased significantly compared with control rats (1.1+/-0.4) nmol/g, but cGMP level was not altered before and after ischemia-reperfusion in either group. It was also revealed that in isolated rat hearts perfused, myocardial function recovered better in IHA rats than that in normoxic control rats. IHA adaptation increased the tolerance of rat hearts against subsequent ischemia-reperfusion injury, and increase in coronary circulation and angiogenesis might be the mechanisms of myocardium protected by IHA.
    Acta Pharmacologica Sinica 04/2002; 23(4):305-10. · 2.91 Impact Factor
  • Yi Zhang · Ning Zhong · Z N Zhou ·
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    ABSTRACT: Although it has been reported that intermittent hypoxia had the anti-arrhythmia effect, little is known about the effects on the action potential (AP) and contraction of papillary muscle, as well as the mechanism of anti-arrhythmia. The purpose of present study is to observe the effects of intermittent hypoxia on action potential and contraction of papillary muscle in rat left ventricle simultaneously using conventional intracellular microelectrode and contraction recording. The effects of intermittent hypoxia on AP and contraction during ischemic solution perfusion were also investigated. After exposed to intermittent hypoxia (six hours daily) for 42 days (IH42), duration (APD20) of 20%, 50% (APD50) and 90% (APD90) repolarization of AP prolonged significantly compared with animals in control (Con). Effective refractory period (ERP) in IH42 also prolonged significantly. Perfused with mimic ischemic solution, the changes of electric and mechanical activities in IH42 and in 28 days exposure to intermittent hypoxia (IH28) were much smaller than that in Con and IH14. The result of the study suggested that intermittent hypoxia prolonged the APD and ERP, offered the resistance against the ischemic damage on myocardium, which may be the electrophysiological basis of the anti-arrhythmia of intermittent hypoxia.
    Life Sciences 11/2000; 67(20):2465-71. DOI:10.1016/S0024-3205(00)00832-8 · 2.70 Impact Factor
  • N Zhong · Y Zhang · H F Zhu · Z N Zhou ·
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    ABSTRACT: In the present study, polymerase chain reaction (PCR) was conducted to determine mtDNA(4834) deletion, and myocardial ultrastructure was visualized by electron microscope to see whether intermittent hypoxia (high altitude) adaptation exerts some action on mitochondria against ischemia/reperfusion injury. Myocardial ischemia/reperfusion in isolated perfused rat hearts induced severe damage to the ultrastructure of myocardial mitochondria and mtDNA4834 deletion down to 87.5% of normoxia rats. After the rats were exposed to intermittent hypoxia (5000 m; 6 h/d for 28 d), the myocardial structure was well reserved and mtDNA(4834) deletion dropped to 28.57%of control (P<0.05). It is suggested that intermittent hypoxia adaptation prevents mtDNA deletion, and preserves normal structure of mitochondria, which would be beneficial to the maintenance of normal mitochondrial function, and increases tolerance of myocardium against ischemia/reperfusion injury.
    Sheng li xue bao: [Acta physiologica Sinica] 10/2000; 52(5):375-80.
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    Y Zhang · N Zhong · Z N Zhou ·
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    ABSTRACT: To study the effects of estradiol (Est) on antiarrhythmic and antioxidative effects of intermittent hypoxia in rat heart. Ligating and loosening the coronary artery of rat to induce ischemic and reperfusion arrhythmias, using arrhythmia score (AS) to evaluate the arrhythmias, measuring the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in myocardium. AS of arrhythmia induced by ischemia and reperfusion in intermittent hypoxia 28-d group (IH28) and in intermittent hypoxia with Est group (IH14-Est) are lower than that in control group (CON), respectively. AS of ischemic arrhythmia but not reperfusion arrhythmia in Est treated group (ESTG) was lower than that in CON. No significant difference in AS of ischemia and reperfusion existed among CON, vehicle group (VEH), and intermittent hypoxia 14-d group (IH14). The activity of SOD was higher and the content of MDA was lower in IH28 and in IH14-Est compared with that in CON. No significant difference of the activity of SOD and the content of MDA existed among CON, VEH, IH14, and ESTG. Est potentiated the antiarrhythmic and antioxidative effects of intermittent hypoxia on rat heart.
    Acta Pharmacologica Sinica 08/2000; 21(7):609-12. · 2.91 Impact Factor
  • N Zhong · Y Zhang · Q Z Fang · Z N Zhou ·
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    ABSTRACT: To quantify the levels of HSP70 induced by different durations of intermittent (high altitude) hypoxia and to correlate them with the degree of protection of the rat heart from ischemic injury. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the level of HSP70 mRNA expression in rat myocardium. Ischemia/reperfusion injury was presented as severity of arrhythmias induced by occlusion and reperfusion of the left anterior descending coronary artery of rat heart. The level of HSP70 mRNA expression increased progressively along with the duration of intermittent hypoxia training. It was 2.6, 3.6, and 3.8 folds after 14-, 28-, and 42-d exposures compared to that of normoxia. The tolerance of rat heart to ischemia/reperfusion injury increased with hypoxia pretreatment. Such an effect was significant after rat were exposed to a 28-d intermittent hypoxia (IH). The scores for ischemia and reperfusion inducing arrhythmia for 28- and 42-d IH were 1.2 +/- 0.5, 1.0 +/- 0.5 and 1.0 +/- 0.5, 0.9 +/- 0.5 (P < 0.01 compared with 4.0 +/- 0.7, 3.3 +/- 0.6 in normoxia rats). The overexpression of HSP70 and the increased tolerance to subsequent acute ischemia/reperfusion injury could last for 2 wk after the rats (subjected to 28 d IH) returned to normoxia. Furthermore, there was a reverse correlation between the amount of HSP70 induced and the arrhythmia occurrence (r = -0.98, -0.92 for ischemia and reperfusion induced arrhythmia, P < 0.01). These results suggest that increased resistance of rat heart to ischemia/reperfusion injury after intermittent hypoxia exposure may be related to the amount of HSP70 induced.
    Acta Pharmacologica Sinica 06/2000; 21(5):467-72. · 2.91 Impact Factor
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    Y Zhang · N Zhong · H F Zhu · Z N Zhou ·
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    ABSTRACT: The purpose of the study was to observe the effects of intermittent hypoxia exposure (IH) on the arrhythmia and antioxidation with ligation of coronary artery of rat heart together with measuring SOD (superoxide dismutase) and MDA (malondialdehyde) in myocardium. Comparison with continued hypoxia exposure was also made. The results obtained are as follows. (1) Arrhythmia scores of ischemic arrhythmia and reperfusion arrhythmia observed in the rats treated with IH 28-day (IH28) and 42-day (IH42), one week (IH28-1W) and two weeks (IH28-2W) after 28-day IH, as well as in those with continued hypoxia 28-day (CH28) and 42-day (CH42), were significantly lower than controls. (2) SOD in IH28, IH42, CH28, CH42, IH28-1W, IH28-2W and three weeks after 28-day IH were significantly higher than controls; MDA in IH14, IH28, IH42, CH28, CH42, IH28-1W and IH28-2W were significantly lower than controls. It is suggested that IH for 28 or 42 days has some definite antiarrhythmic effect against ischemia and reperfusion, which was related to the strength of antioxidation in myocardium. The antiarrhythmic effects occurred gradually after 14 days IH and persisted for about two weeks after 28 days IH.
    Sheng li xue bao: [Acta physiologica Sinica] 05/2000; 52(2):89-92.
  • N Zhong · Q.Z. Fang · Y Zhang · J.Q. Qian · Z.N. Zhou ·
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    ABSTRACT: To study the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenyl-ethylamino) propane hydrochloride (DDPH) on action potential (AP), inward rectifier K+ current (IK1), and delayed rectifier K+ current (IK) in isolated guinea pig ventricular myocytes. Whole cell patch-clamp recording techniques. DDPH 0.1-100 mumol.L-1 decreased 50% duration of action potential (APD50) concentration-dependently. APD50 was shortened from (493 +/- 58) to (262 +/- 38) ms (n = 7 cells from 5 guinea pigs, P < 0.01) by DDPH 10 mumol.L-1. However, 90% duration of action potential (APD90) was increased by DDPH (> 1 mumol.L-1). At high concentration (> 10 mumol.L-1) DDPH decreased resting membrane potential (RP) and amplitude of action potential (APA). DDPH inhibited tail current of IK (IK.tail) concentration-dependently, 46% at 10 mumol.L-1 and 78% at 100 mumol.L-1. EC50 for DDPH inhibiting IK was 13.3 (11.6-16.7) mumol.L-1. DDPH also blocked IK1. DDPH at high concentration (> 10 mumol.L-1) shifted the reverse potential of IK1 positively. All the effects of DDPH were reversible after washout. DDPH blocked both IK1 and IK current in guinea pig ventricular myocytes.
    Acta Pharmacologica Sinica 05/2000; 21(4):301-5. · 2.91 Impact Factor
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    N Zhong · Q Z Fang · Y Zhang · Z N Zhou ·
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    ABSTRACT: To characterize the properties of chloride currents and its modulation in human umbilical vein endothelial cells (HUVEC). Using whole-cell patch-clamp recording techniques. Exposure of HUVEC to 13.5% and 27% hypotonic solution (HTS) induced a current ICl, vol. This current was correlated with the changes in cell volume and showed a modest outward rectification. It was slowly inactivated at positive potential (> 50 mV), and it was time- and voltage-independent in kinetics. The current densities (pA/pF) were 20 +/- 3 (13.5% HTS) and 58 +/- 4 (27% HTS, n = 7), respectively at +100 mV test potential. Applying GTP gamma s (300 mumol.L-1) elicited a current similar to ICl, vol, while cAMP (0.5 mmol.L-1) had no effect on the current. Increase in [Ca2+]i, either by directly loading cells with high concentration of Ca2+ (CaCl2), or by perfusing vasoactive agonist ATP (10 mumol.L-1), activated ICl, Ca. The current density was only (23 +/- 5) pA/pF (n = 8 cells). Such current was slowly activated at positive potential, inactivated quickly at negative potential, and showed strong outward rectification. Both currents were inhibited by DIDS and verapamil. Challenging a cell with elevated [Ca2+]i and HTS activated ICl, vol on the top of ICl, Ca in the same cell, suggested co-existence of these two currents and that they were modulated by different ways. cAMP-regulated chloride channel and ClC (chloride channel family) channel were absent. HUVEC express two kinds of chloride channels, ICl, vol activated by change in cell volume and ICl, Ca by elevation of [Ca2+]i, respectively.
    Acta Pharmacologica Sinica 03/2000; 21(3):215-20. · 2.91 Impact Factor
  • N Zhong · J Q Qian ·
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    ABSTRACT: To investigate the influence of selective antagonist for muscarinic (M) receptor subtype on tetrandrine (Tet) reducing heart rate, inhibiting sinoatrial node (SAN) function, and its ionic mechanism. Effects of reducing heart rate of Tet were maintained in isolated right atrium and pithed rats. Modification on action potentials (AP) of SAN cells and L-type calcium current (ICa-L) by Tet were recorded by means of standard microelectrode and patch-clamp whole cell recording techniques. Tet inhibited spontaneous beating rate of isolated right atrium (EC50, 23.7 mumol.L-1) and reduced heart rates in pithed rats in a concentration-dependent manner (EC50, 18.6 Automaticity of SAN was inhibited by Tet. AP upstroke velocity (Vmax), spontaneous depolarization rates in phase 4 (SP4) were decreased and sinus cycle length (SCL) was prolonged when treated with Tet. Tet (30 mumol.L-1) caused a reduction in peak value of ICa-L from (1275 +/- 190) pA to (498 +/- 94) pA in isolated single cardiomyocyte. Atropine and AF-DX 116 (M2 subtype selective antagonist) could attenuate such effects of Tet in a competitive mode. Negative chronotropic effects of Tet are due to its inhibition of ICa-L. Modification on ICa-L is the major mechanism of M receptor modulating Tet effects.
    Zhongguo yao li xue bao = Acta pharmacologica Sinica 01/2000; 20(12):1068-72.

Publication Stats

169 Citations
21.66 Total Impact Points


  • 2010
    • University of California, San Francisco
      San Francisco, California, United States
  • 2008
    • Hebei Medical University
      Chentow, Hebei, China
  • 2002-2004
    • University of California, Berkeley
      • Department of Molecular and Cell Biology
      Berkeley, California, United States
  • 2000
    • Shanghai Institute of Technology
      Shanghai, Shanghai Shi, China
    • Chinese Academy of Sciences
      • Institute of Plant Physiology and Ecology
      Peping, Beijing, China