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1.
Acta Academiae Medicinae Sinicae ; (6): 108-116, 2020.
Artigo em Chinês | WPRIM | ID: wpr-793055

RESUMO

G protein-gated inward rectifier potassium(GIRK)channels are widely distributed in the central nervous system and play important roles in maintaining the resting membrane potential of neurons,adjusting neuronal excitability,and regulating the release of neurotransmitter.Studies have shown that addictive behavior is closely related to the expression and activity of the GIRK channels in the brain reward system and the GIRK channels may be a potential target for addiction treatment.This article summarizes the recent research advances in GIRK channels in terms of structure,intracranial tissue distribution,and especially substance addiction.

2.
The Korean Journal of Physiology and Pharmacology ; : 111-119, 2020.
Artigo em Inglês | WPRIM | ID: wpr-787133

RESUMO

In vascular smooth muscle, K⁺ channels, such as voltage-gated K⁺ channels (Kv), inward-rectifier K⁺ channels (Kir), and big-conductance Ca²⁺-activated K⁺ channels (BK(Ca)), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (I(Kv) and I(Kir)) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) I(Kv) was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) I(Kv) inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) I(Kir) was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) I(BKCa) did not differ between branches. Moreover, in PAH rats, I(Kir) and I(Kv) decreased in SCSMCs, but not in RCSMCs or LCSMCs, and I(BKCa) did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in I(Kv) and I(Kir) occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller I(Kir) in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular K⁺ concentration under increased activity of the myocardium.


Assuntos
Animais , Ratos , Vasos Coronários , Cardiopatias , Insuficiência Cardíaca , Hiperemia , Hipertensão , Hipertrofia Ventricular Direita , Isquemia , Potenciais da Membrana , Monocrotalina , Músculo Liso , Músculo Liso Vascular , Miocárdio , Miócitos de Músculo Liso , Técnicas de Patch-Clamp , Canais de Potássio , Septo do Cérebro
3.
Chinese Journal of Pathophysiology ; (12): 206-211, 2019.
Artigo em Chinês | WPRIM | ID: wpr-744228

RESUMO

AIM:To investigate the protective effect of zacopride (ZAC) on the pressure-overload left ventricular remodeling in the rats induced by coarctation of abdominal aorta.METHODS:Male Sprague-Dawley (SD) rats with pressure overload were induced by the coarctation of abdominal aorta.The model rats were intraperitoneally administered with ZAC, chloroquine (Chlor) , and zacopride+chlorquine (ZAC+Chlor).The study duration was 8 weeks.The cardiac structure and function were assessed by echocardiography.The heart weight/body weight (HW/BW) ratio and the left ventricular weight/body weight (LVW/BW) ratio were calculated.The changes of structure and shape in myocardial tissue were observed with HE staining.The ultrastructure of the myocytes was observed under transmission electron microscope.The inward rectifier potassium channel (IK1) protein expression was determined by Western blot.The mRNA expression of Kir2.1 was detected by RT-PCR.RESULTS:Compared with vehicle group, ZAC improved cardiac function, as indicated by the decreased left ventricular end-diastolic dimension (LVEDD) and left ventricular end systolic dimension (LVESD) (P<0.05) , and the increased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) (P<0.01).The HW/BW and LVW/BW ratios were significantly decreased, and the cross-sectional area of the cardiomyocytes was significantly less in ZAC group than that in vehicle group (P<0.01).The ultrastructure of the myocytes was significantly improved.Chlor blocked the protective effect of zacopride on the pressure-overload left ventricular remodeling.The protein level ofmRNA expression of Kir2.1 in the cardiac tissues in ZAC group were significantly increased compared with vehicle group (P<0.01).CONCLUSION:ZAC significantly attenuates pressure overload-induced ventricular remodeling in rats.

4.
Chinese Journal of Pharmacology and Toxicology ; (6): 534-540, 2017.
Artigo em Chinês | WPRIM | ID: wpr-611116

RESUMO

OBJECTIVE To compare the effect of four 5-hydroxytryptamine type 4 (5-HT4) receptor agonists:cisapride,zacopride,macopride and 2-[1-(4-piperonyl) piperazinyl]-benzothiazole (BZTZ),on rat cardiac inward rectifier potassium channel (IK1)and heart rhythm.METHODS The whole-cell configuration of patch-clamp technique was used to record effects of 5-HT4 receptor agonists onIk1 in enzymatic dissociated rat ventricular myocytes or Kir2.1 transfected HEK 293 cells.Western blotting was used to observe the expression of Kir2.1 channel exposed 24 h to agents in ventricular myocytes.Langendorff-perfused hearts were perfused with four agents respectively for 30 min.The electrocardiogram was recorded simultaneously.RESULTS BZTZ,cisapride and mosapride 0.1-10 μmol· L-1 decreasedIk1 in a concentrationdependent manner.At the same concentration (1 μmol· L-1),BZTZ showed the most potent inhibition onIκ1 (P<0.01),followed by cisapride.Mosapride showed slight inhibition efficiency.However,zacopride enhanced Iκ1 (P<0.01).In Kir2.1 heterologous expression systems,zacopride activated Kir2.1 current (P<0.01) while mosapride had no effect.In ex vivo Langendorff-perfused hearts,BZTZ and cisapride 1μmol· L-1 elicited singnificant rhythm disturbances,and the total of premature ventricular beats (PVB) were 159±28 and 61±13.50% (4/8) (P<0.05) and 25% (1/8) of the hearts exhibited ventricular tachycardia (VT),while 37.5% (3/8) and 12.5% (1/8) of the hearts exhibited ventricular fibrillation (VF),respectively.Mosapride and zacopride had no side effects on heart rhythm.Zacopride also suppressed BZTZ-or cisapride-induced arrhythmias.BZFZ had the strongest proarryhthmic potency among the 5-HT4 agonists,followed by cisapride,mosapride and zacopride.CONCLUSION Iκ1 might be an independent risk factor for arrhythmogenesis and a new target for screening safe 5-HT4 receptor agonists and gastrointestinal prokinetic agents.

5.
Chinese Journal of Pathophysiology ; (12): 1371-1378, 2017.
Artigo em Chinês | WPRIM | ID: wpr-608989

RESUMO

AIM: To investigate the effect of zacopride, an inward rectifier potassium channel agonist, on ouabain-induced arrhythmias in adult rats, and to explore the underlying electrophysiological mechanism.METHODS: Using ouabain to establish in vitro and in vivo arrhythmic rat models, the effects of zacopride on ouabain-induced arrhythmias were observed.The technique of whole-cell patch clamp was used to observe the effects of zacopride on inward rectifier potassium current (IK1), resting membrane potential (RMP) and delayed afterdepolarizations (DADs) in single rat ventricular myocyte.RESULTS: Zacopride at 1 μmol/L significantly reduced total number of premature ventricular beats, and the duration and incidence of ventricular tachycardia and ventricular fibrillation induced by ouabain in rat hearts in vitro (P<0.05).In anesthetized rats, zacopride at 15 μg/kg significantly reduced total number of premature ventricular beats, and the duration and incidence of ventricular tachycardia and ventricular fibrillation induced by ouabain (P<0.05).IK1 was significantly inhibited by ouabain (P<0.05), which was partially and even completely reversed by zacopride at 0.1~10 μmol/L.RMP value was significantly reduced by ouabain (P<0.05), and then increased to different levels after treatment with zacopride (0.1~10 μmol/L).Zacopride at 1 μmol/L showed its maximal effect and RMP was restored to normal level.Moreover, zacopride at 1 μmol/L markedly suppressed ouabain-induced DADs in single rat ventricular myocyte.The incidence of DADs decreased from 91.67% to 12.50% after zacopride was applied (P<0.05), and this effect was abolished by 1 μmol/L BaCl2.CONCLUSION: Inward rectifier potassium channel agonist zacopride significantly inhibits ouabain-induced ventricular arrhythmias in adult rats.The mechanism is related to increased RMP level and inhibition of DADs by activation of IK1 channel.

6.
Chinese Pharmacological Bulletin ; (12): 641-646, 2017.
Artigo em Chinês | WPRIM | ID: wpr-615941

RESUMO

Aim To examine the effect of zacopride,a specific inward rectifier potassium channel(IK1)agonist,on L-thyroxine(T4)-induced ventricular remodeling and the underlying mechanism.Methods SD rats were randomly divided as control,L-thyroxine(L-thy,1 mg·kg-1·d-1,ig,10 d)model,L-thy +zacopride(5,15,50 μg·kg-1,respectively,ip),L-thy+zacopride(15 μg·kg-1)+chloroquine(7.5 μg·kg-1,ip)and L-thy+captopril(100 mg·kg-1·d-1,drinking water)groups.Echocardiography and cardiac hypertrophic indexes were measured to confirm the establishment of the ventricular remodeling model.The changes of IK1 and L-calcium current(ICa-L)were detected by whole cell patch clamp technique.The confocal microscopy and fluorescent indicator Fluo-4 were applied to examine the intracellular Ca2+ concentration([Ca2+]i)of isolated adult rat ventricular myocytes.Results L-thyroxine induced left ventricular hypertrophy with increased ratio of heart weight(HW)to body weight(HW·BW-1),ratio of left ventrical weight(LVW)to body weight(LVW·BW-1),left ventricular dimension in diastole(LVIDd),left ventricular dimension in systole(LVIDs),interventricular septum thickness(IVS)and decreased ejection fraction(EF),fractional shortening(FS)(P<0.01).Patch clamp data suggested IK1 was downregulated,while ICa-L was upregulated(P<0.01).In isolated adult cardiomyocytes,L-thyroxine increased the cell area and [Ca2+]i(P<0.01).Zacopride treatment obviously alleviated cardiac remodeling,improved cardiac function,reversed the changes of IK1 and ICa-L,and significantly attenuated intracellular calcium overload(P<0.01).The optimum dose of zacopride in vivo was 15 μg·kg-1 at which the effect was compared favourably with captopril,a classical anti-remodeling agent.Low-dose IK1 atagonist chloroquine could reverse the effect of zacopride(P<0.01).Conclusion Via activating IK1,zacopride could significantly decrease Ca2+ influx and intracellular calcium overload thereby inhibiting L-thyroxine-induced cardiac ventricular remodeling.

7.
Chinese Pharmacological Bulletin ; (12): 1127-1132,1133, 2016.
Artigo em Chinês | WPRIM | ID: wpr-604465

RESUMO

Aim To investigate the effect of zacopride ( Zac) on cardiac arrhythmia in isoproterenol ( ISO)-in-duced myocardial hypertrophic rats and the underlying electrophysiological mechanisms .Methods ① Fifty-one rats were randomly divided into control group ( n=17 ) , ISO group ( n=17 ) and ISO +Zac group ( n =17 ) .Rat model with cardiac arrhythmia and hypertro-phy was established by intraperitoneal ISO ( 5 mg?kg -1 ) injection.②ECGs were recorded to observe the effects of Zac on arrhythmia in model rats .③ Whole-cell patch clamp was applied to record inwardly rectifi-er potassium current(IK1), resting membrane potential ( RMP ) and amplicated delayed afterdepolarizations (DADs).Results ① Echocardiographic examination showed that , left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) significantly decreased in rats in ISO group compared with control group , whereas left ventricular posterior wall end-diastolic thickness ( LVPWd) and in-terventricular septum end-diastolic thickness ( IVSd ) increased ( P<0.05 ) , suggesting rat model of isoprot-erenol-induced myocardial hypertrophy was successfully established .② ECGs showed that 88.89% of rats in ISO group had ventricular premature beats ( VPBs ) , which significantly decreased to 11.11% after the ap-plication of Zac ( P <0.05 ) .③ Values of RMP de-creased from ( -71.05 ±1.27 ) mV in control group to (-69.38 ±1.21 ) mV in ISO group ( P<0.05 ) . After Zac administration , RMP significantly increased to ( -73.86 ±1.33 ) mV compared with control and ISO group(P<0.05).④DADs and TA incidence sig-nificantly decreased from 88.24% in ISO group to 11.76%in ISO+Zac group ( P<0.05 ) .⑤ Compared with control group , IK1 density was markedly reduced in ISO group, whereas Zac could effectively rescue IK1 suppression to normal level .Conclusions Zac, as a selective IK1 channel agonist , can significantly inhibit cardiac arrhythmia in isoproterenol-induced myocardial hypertrophic rats , which is mainly attributed to in-creased RMP by enhancing IK1 and subsequent suppres-sion of DADs.

8.
Chinese Pharmacological Bulletin ; (12): 1081-1084,1085, 2015.
Artigo em Chinês | WPRIM | ID: wpr-602335

RESUMO

Aim To investigate the inhibitory effects of zacopride(Zac) on arrhythmia induced by isoproterenol ( ISO) and the underlying mechanisms in rats. Meth-ods ①ECGs were recorded in anesthetized rats in vi-vo to observe the effects of zacopride on arrhythmia in-duced by ISO. ② Intracellular microelectrode tech-nique was used to investigate the effects of zacopride on resting membrane potential, delayed afterdepolariza-tions ( DADs) and triggered activity ( TA) induced by ISO combined with 3. 6 mmol·L-1 CaCl2 in right ven-tricular papillary muscle of rats. Results ① In ISO group rats, ventricular premature beats ( VPB ) oc-curred frequently with ST-segment depression. Com-pared with ISO group, the incidence of VPB in ISO+Zac group decreased from 100% to 50% ( n=6 , P<0. 05 ) and the total number of VPB recorded in 1 hour significantly reduced from 1 574 ± 521 to 33 ± 40 ( n=6,P<0. 05). ② Zacopride at 1 μmol·L-1 could hy-perpolarize the resting membrane potential of right ven-tricular papillary muscle in normal rat from ( -74. 42 ± 1. 95 ) mV to ( -78. 50 ± 2. 07 ) mV ( n =6 , P <0. 05). ③ Zacopride at 1 μmol·L-1 significantly de-pressed the DADs and TA induced by ISO combined with 3. 6 mmol·L-1 CaCl2 in right ventricular papilla-ry muscle. The incidence of DADs decreased from 93. 75% in rats in ISO group to 25% in ISO +Zac group ( n =16 , P <0. 05 ) , and this antiarrhythmic effect could be reversed by 1 μmol·L-1 BaCl2 . Conclusions Zacopride, a selective IK1 channel ago-nist , can significantly inhibit cardiac arrthymia induced by ISO in rats, the mechanism of which is mainly at-tributed to zacopride-induced hyperpolarization of the resting membrane potential and subsequent suppression of DADs and TA via enhancing IK1 . These results pro-vide further evidence that to enhance IK1 moderately may be a feasible pathway for antiarrthymic therapy.

9.
Chinese Pharmacological Bulletin ; (12): 461-465, 2010.
Artigo em Chinês | WPRIM | ID: wpr-403003

RESUMO

Aim To investigate the effects of 5-HT_4 receptor agonist and 5-HT_3 receptor antagonist 2-[1-(4-piperonyl)piperazinyl]benzothiazole on rat heart rhythm and the involved ionic mechanisms.Methods Langendorff-perfused rat hearts were subjected to 0.1~10 μmol·L~(-1) 2-[1-(4-piperonyl)-piperazinyl]benzothiazole for 15 minutes with simultaneous ECGs recording.The whole-cell patch-clamp electrophysiology was used to record effects of 2-[1-(4-piperonyl)piperazinyl]benzothiazole on inward rectifier K~+ current(I_(K1)),transient outward K~+ current(I_(to)),resting membrane potential(RMP)and action potential(AP)in enzymatic dissociated rat ventricular myocytes.Results In ex vivo Langendorff-perfused hearts,0.1~10 μmol·L~(-1) 2-[1-(4-piperonyl)piperazinyl]benzothiazole elicited singnificant rhythm disturbances.In the presence of 10 μmol·L~(-1) agent,the total of PVB were 236±37,87.5%(7/8)hearts exhibited VT,and 62.5%(5/8)hearts exhibited VF(P<0.01).At the concentration of 0.1~10 μmol·L~(-1),2-[1-(4-piperonyl)piperazinyl]benzothiazole could inhibit I_(K1)(EC50=0.74 μmol·L~(-1))and I_(to)(EC50=2.16 μmol·L~(-1)),decrease RMP and prolong action potential duration(APD)in concentration-dependent manners(n=6,P<0.01).Conclusion Inhibition of IK1,Ito and resultant prolongation of APD,depolarization of RMP might be the critical causes for induction of arrhythmias by 2-[1-(4-piperonyl)piperazinyl]benzothiazole in rat.

10.
The Korean Journal of Physiology and Pharmacology ; : 61-70, 2009.
Artigo em Inglês | WPRIM | ID: wpr-728654

RESUMO

We have examined the effects of certain mutations of the selectivity filter and of the membrane helix M2 on Ba2+ blockage of the inward rectifier potassium channel, Kir 2.1. We expressed mutant and wild type murine Kir 2.1 in Chinese hamster ovary (CHO) cells and used the whole cell patch-clamp technique to record K+ currents in the absence and presence of externally applied Ba2+. Wild type Kir2.1 was blocked by externally applied Ba2+ in a voltage and concentration dependent manner. Mutants of Y145 in the selectivity filter showed little change in the kinetics of Ba2+ blockage. The estimated Kd(0) was 108micrometer for Kir2.1 wild type, 124micrometer for a concatameric WT-Y145V dimer, 109micrometer for a WT-Y145L dimer, and 267micrometer for Y145F. Mutant channels T141A and S165L exhibit a reduced affinity together with a large reduction in the rate of blockage. In S165L, blockage proceeds with a double exponential time course, suggestive of more than one blocking site. The double mutation T141A/S165L dramatically reduced affinity for Ba2+, also showing two components with very different time courses. Mutants D172K and D172R (lining the central, aqueous cavity of the channel) showed both a decreased affinity to Ba2+ and a decrease in the on transition rate constant (kon). These results imply that residues stabilising the cytoplasmic end of the selectivity filter (T141, S165) and in the central cavity (D172) are major determinants of high affinity Ba2+ blockage in Kir 2.1.


Assuntos
Animais , Cricetinae , Feminino , Cricetulus , Citoplasma , Cinética , Membranas , Ovário , Técnicas de Patch-Clamp , Canais de Potássio , Canais de Potássio Corretores do Fluxo de Internalização
11.
Yonsei Medical Journal ; : 459-471, 2008.
Artigo em Inglês | WPRIM | ID: wpr-79505

RESUMO

PURPOSE: This study examined the expression and function of inward rectifier K+ channels in cultured rat hepatic stellate cells (HSC). MATERIALS AND METHODS: The expression of inward rectifier K+ channels was measured using real-time RT-PCR, and electrophysiological properties were determined using the gramicidin-perforated patch-clamp technique. RESULTS: The dominant inward rectifier K+ channel subtypes were K(ir)2.1 and K(ir)6.1. These dominant K+ channel subtypes decreased significantly during the primary culture throughout activation process. HSC can be classified into two subgroups: one with an inward-rectifying K+ current (type 1) and the other without (type 2). The inward current was blocked by Ba2+ (100micrometer) and enhanced by high K+ (140mM), more prominently in type 1 HSC. There was a correlation between the amplitude of the Ba2+-sensitive current and the membrane potential. In addition, Ba2+ (300micrometer) depolarized the membrane potential. After the culture period, the amplitude of the inward current decreased and the membrane potential became depolarized. CONCLUSION: HSC express inward rectifier K+ channels, which physiologically regulate membrane potential and decrease during the activation process. These results will potentially help determine properties of the inward rectifier K+ channels in HSC as well as their roles in the activation process.


Assuntos
Animais , Masculino , Ratos , Bário/farmacologia , Western Blotting , Células Cultivadas , Eletrofisiologia , Fígado/citologia , Potenciais da Membrana/efeitos dos fármacos , Potássio/farmacologia , Canais de Potássio Corretores do Fluxo de Internalização/genética , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase Via Transcriptase Reversa
12.
Korean Journal of Anesthesiology ; : 557-566, 2006.
Artigo em Coreano | WPRIM | ID: wpr-152185

RESUMO

BACKGROUND: Desflurane has been reported to prolong the QTc. Several ionic currents that contribute to the prolongation of the action potential (AP) duration were investigated using guinea pig (GP) and rat ventricular myocytes. METHODS: The normal APs were measured in isolated GP papillary muscles at 37 degrees C. Ventricular myocytes were obtained from GP and rat hearts. Both the delayed outward K+ current (I(K)) and the inward rectifier K+ current (I(KI)) were assessed using a voltage ramp protocol. A more detailed study on the I(K) was performed. The ICa, L was measured. In the rat ventricular myocytes, the transient outward K+ current (I(to)) was obtained. All the patch clamp experiments were carried out at room temperature. The values are presented as mean +/- SD. RESULTS: 0.91 mM desflurane significantly prolonged the APD in the GP ventricular myocytes. Using a linear voltage ramp protocol, the I(KI) at -130 mV and the peak outward I(KI) at -60 to -50 mV were not found to be significantly reduced by 0.78 and 1.23 mM desflurane, respectively. However, the peak outward I(K) at +60 mV was significantly reduced to 63 +/- 19% and 58 +/- 12% of the baseline by 0.78 and 1.23 mM desflurane, respectively. At a membrane potential of +60 mV, 0.78 and 1.23 mM desflurane reduced the Ito to 80 +/- 8% and 68 +/- 7%, respectively. A concentration-dependent reduction in the ICa, L was observed. CONCLUSIONS: The prolongation of the APD induced by clinically relevant concentrations of desflurane in GP and rat ventricular myocytes is most likely the result of I(K) and I(to) suppression.


Assuntos
Animais , Ratos , Potenciais de Ação , Acessibilidade Arquitetônica , Cobaias , Coração , Potenciais da Membrana , Células Musculares , Músculos Papilares
13.
The Korean Journal of Physiology and Pharmacology ; : 741-748, 1997.
Artigo em Inglês | WPRIM | ID: wpr-727957

RESUMO

In the present study, we have investigated the effect of metabolic inhibition on the inward rectifer K current (IK1). Using whole cell patch clamp technique we applied voltage ramp from +80 mV to -140 mV at a holding potential of -30 mV and recorded the whole cell current in single ventricular myocytes isolated from the rabbit heart. The current-voltage relationship showed N-shape (a large inward current and little outward current with a negative slope) which is a characteristic of IK1. Application of 0.2 mM dinitrophenol (DNP, an uncoupler of oxidative phosphorylation as a tool for chemical hypoxia) to the bathing solution with the pipette solution containing 5 mM ATP, produced a gradual increase of outward current followed by a gradual decrease of inward current with little change in the reversal potential (-80 mV). The increase of outward current was reversed by glibenclamide (10 muM), suggesting that it is caused by the activation of KATP. When DNP and glibenclamide were applied at the same time or glibenclamide was pretreated, DNP produced same degree of reduction in the magnitude of the inward current. These results show that metabolic inhibition induces not only the increase of KATP channel but also the decrease of IK1. Perfusing the cell with ATP-free pipette solution induced the changes very similar to those observed using DNP. Long exposure of DNP (30 min) or ATP-free pipette solution produced a marked decrease of both inward and outward current with a significant change in the reversal potential. Above results suggest that the decrease of IK1 may contribute to the depolarization of membrane potential during metabolic inhibition.


Assuntos
Trifosfato de Adenosina , Acessibilidade Arquitetônica , Banhos , Glibureto , Coração , Potenciais da Membrana , Células Musculares , Fosforilação Oxidativa
14.
Chinese Journal of Pathophysiology ; (12)1989.
Artigo em Chinês | WPRIM | ID: wpr-534153

RESUMO

0.05).Zacopride at concentration of 1.0 ?mol/L showed the most potent activity on IK1 with approximately 30% increment both in inward current and outward current(P

15.
Chinese Pharmacological Bulletin ; (12)1987.
Artigo em Chinês | WPRIM | ID: wpr-678719

RESUMO

Kir2 1. Moreover, drop of pHi reduced the M 1 induced inhibition of Kir3 1/3 4 currents, and enhanced the desensitization of M 2 induced Kir3 1/3 4 activation. CONCLUSION The basal currents and M receptor induced currents of Kir3 1/3 4 can be regulated by intracellular pH. These changes may play some important roles in pathophysiological conditions like cardiac ischemia.

16.
Medical Journal of Chinese People's Liberation Army ; (12)1983.
Artigo em Chinês | WPRIM | ID: wpr-556502

RESUMO

Objective To investigate the changes of action potential duration (APD) and transient outward K + current (I to) and inward rectifier K + current(I K1) of ventricular myocytes after 3 weeks of myocardial infarction, and to inquire into the effect of bisoprolol. Methods APD was recorded with microelectrode. Ventricular myocytes were singly isolated from rabbit heart using modified Langendoff perfusion and soaked with collagenase. I to and I K1 of single rabbit ventricular myocytes were recorded by whole-cell path-clamp technique. Results Both APD 50 and APD 90 of the cell from noninfarcted region in MI group were markedly longer than that in sham group (P

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