Objectives To investigate the effects of β2-adrenergic antagonist on cytosolic Ca^2 ＋ （[Ca^2＋ ]i） in ventricular myocytes from infarcted rat heart. Methods A ligature was placed around left anterior descending co...Objectives To investigate the effects of β2-adrenergic antagonist on cytosolic Ca^2 ＋ （[Ca^2＋ ]i） in ventricular myocytes from infarcted rat heart. Methods A ligature was placed around left anterior descending coronary artery of rat hearts. Rats in the control group were sham-operated. Cardiomyocytes were dissociated at two, four, eight weeks after myocardial infarction （MI） and [Ca^2＋]i was measured via fura-2 fluorescence. The response of cardiomyocytes to isoproterenol in presence or absence of betal-adrenergic antagonist atenolol, beta2-adrenergic antagonist ICI118, 551 or non-selective β1, 2- adrenergic antagonists propranolol was examined. Results The followings were found that ICI 118, 551 had no significant effects on the rise of [Ca^2＋]i induced by isoproterenol in normal ventricular myocytes （P 〉 0.05）, ICI118, 551 only significantly attenuated the rise of [Ca^2＋]i induced by isoproterenol at four weeks and eight weeks after MI （24.5%±5.7% vs 57.8% ± 13.2%, P〈 0.01; 12.2%±7.9% vs 44.6%±11.3%, P〈 0.01）. Atenolol had suppressive effects only in the control group and the post-MI group of two weeks （P 〈 0.05）, and propranolol had suppressive effects in the control and all the three post-MI groups （P 〈 0.01）. Conclusions Beta2-adrenergic antagonist ICI118, 551 may exert negative effects on Ca^2＋ overload initiated by sympathetic stimulation after MI.展开更多
AtPEPTIDE RECEPTOR2 （AtPEPR2） is a member of leucine-rich repeat receptor-like kinase family and binds to a group of AtPROPEP gene-encoded endogenous peptides, AtPeps. Previously, we found that AtPEPR2 plays a moder...AtPEPTIDE RECEPTOR2 （AtPEPR2） is a member of leucine-rich repeat receptor-like kinase family and binds to a group of AtPROPEP gene-encoded endogenous peptides, AtPeps. Previously, we found that AtPEPR2 plays a moderate role in the AtPep1-mediated innate immunity responses in Arabidopsis leaf. In this study, we found that AtPEPR2 promoter has strong activity in the vascular tissues of the roots and the atpepr2 mutants showed a moderate but significantly shorter root phenotype. AtPEPR2 partial y mediated AtPep1-induced root elongation inhibition. AtPep1-triggered cytosolic Ca2t transient rise in roots showed partial dependence on AtPEPR2 and ful y on extracellular Ca2t （[Ca2t]ext）. Transcriptional profiling analysis found that expression of 75% of AtPep1-modulated genes in roots was ful y dependent on AtPEPR2, of which two dramatical y induced genes showed partial dependence on the [Ca2t]ext. Arabidopsis genome contains seven Glutamine Dumpers genes （AtGDUs）, encoding amino acid exporters. Three of them （AtGDU2, 3, 5） were among the top 10 genes that were＆amp;nbsp;downregulated by AtPep1 through AtPEPR2 ful y dependent pathway. Treatment with AtPep1 strongly suppressed pro-moter activity of AtGDU3 in roots, which was relieved by chelating [Ca2t]ext. Arabidopsis overexpressing AtGDU3 showed a shorter root phenotype and decreased sensitivity to the AtPep1-mediated inhibition of root elongation. Taken together, this study demonstrated a significant role of AtPEPR2 in the AtPep1-mediated signaling in the roots.展开更多
Background Preconditioning with remifentanil confers cardioprotection. Since Ca^2＋ overload is a precipitating factor of injury, we determined the effects of remefentanil on intracellular Ca^2＋ （[Ca^2＋]i） and its...Background Preconditioning with remifentanil confers cardioprotection. Since Ca^2＋ overload is a precipitating factor of injury, we determined the effects of remefentanil on intracellular Ca^2＋ （[Ca^2＋]i） and its transients induced by electrical stimulation and caffeine, which reflects Ca^2＋ handling by Ca^2＋ handling proteins, in rat ventricular myocytes. Methods Freshly isolated adult male Sprague-Dawley rat myocytes were loaded with Fura-2/AM and [Ca]i was determined by spectrofluorometry. Remifentanil at 0.1-1000 μg/L was administered. Ten minutes after administration, either 0.2 Hz electrical stimulation was applied or 10 mmol/L caffeine was added. The [Ca^2＋]i, and the amplitude, time resting and 50% decay （t50） of both transients induced by electrical stimulation （E[Ca^2＋]i） and caffeine （C[Ca^2＋]i） were determined. Results Remifentanil （0.1-1000.0 μg/L） decreased the [Ca^2＋]i in a dose-dependent manner. It also decreased the amplitude of both transients dose-dependently. Furthermore, it increased the time to peak and tso of both transients dose-dependently. Conclusion Remifentanil reduced the [Ca^2＋]i and suppressed the transients induced by electrical stimulation and caffeine in rat ventricular myocytes.展开更多
文摘Objectives To investigate the effects of β2-adrenergic antagonist on cytosolic Ca^2 ＋ （[Ca^2＋ ]i） in ventricular myocytes from infarcted rat heart. Methods A ligature was placed around left anterior descending coronary artery of rat hearts. Rats in the control group were sham-operated. Cardiomyocytes were dissociated at two, four, eight weeks after myocardial infarction （MI） and [Ca^2＋]i was measured via fura-2 fluorescence. The response of cardiomyocytes to isoproterenol in presence or absence of betal-adrenergic antagonist atenolol, beta2-adrenergic antagonist ICI118, 551 or non-selective β1, 2- adrenergic antagonists propranolol was examined. Results The followings were found that ICI 118, 551 had no significant effects on the rise of [Ca^2＋]i induced by isoproterenol in normal ventricular myocytes （P 〉 0.05）, ICI118, 551 only significantly attenuated the rise of [Ca^2＋]i induced by isoproterenol at four weeks and eight weeks after MI （24.5%±5.7% vs 57.8% ± 13.2%, P〈 0.01; 12.2%±7.9% vs 44.6%±11.3%, P〈 0.01）. Atenolol had suppressive effects only in the control group and the post-MI group of two weeks （P 〈 0.05）, and propranolol had suppressive effects in the control and all the three post-MI groups （P 〈 0.01）. Conclusions Beta2-adrenergic antagonist ICI118, 551 may exert negative effects on Ca^2＋ overload initiated by sympathetic stimulation after MI.
基金supported by a grant from National Natural Science Foundation of China(31171364)Program for New Century Excellent Talents in University from Ministry of Education(NCET‐10‐0906)+1 种基金Major Basic Science Research Open Program from Inner Mongolia Science and Technology DepartmentStartup Grant from Inner Mongolia University-Hohhot,P.R.China for Z.Q
文摘AtPEPTIDE RECEPTOR2 （AtPEPR2） is a member of leucine-rich repeat receptor-like kinase family and binds to a group of AtPROPEP gene-encoded endogenous peptides, AtPeps. Previously, we found that AtPEPR2 plays a moderate role in the AtPep1-mediated innate immunity responses in Arabidopsis leaf. In this study, we found that AtPEPR2 promoter has strong activity in the vascular tissues of the roots and the atpepr2 mutants showed a moderate but significantly shorter root phenotype. AtPEPR2 partial y mediated AtPep1-induced root elongation inhibition. AtPep1-triggered cytosolic Ca2t transient rise in roots showed partial dependence on AtPEPR2 and ful y on extracellular Ca2t （[Ca2t]ext）. Transcriptional profiling analysis found that expression of 75% of AtPep1-modulated genes in roots was ful y dependent on AtPEPR2, of which two dramatical y induced genes showed partial dependence on the [Ca2t]ext. Arabidopsis genome contains seven Glutamine Dumpers genes （AtGDUs）, encoding amino acid exporters. Three of them （AtGDU2, 3, 5） were among the top 10 genes that were＆amp;nbsp;downregulated by AtPep1 through AtPEPR2 ful y dependent pathway. Treatment with AtPep1 strongly suppressed pro-moter activity of AtGDU3 in roots, which was relieved by chelating [Ca2t]ext. Arabidopsis overexpressing AtGDU3 showed a shorter root phenotype and decreased sensitivity to the AtPep1-mediated inhibition of root elongation. Taken together, this study demonstrated a significant role of AtPEPR2 in the AtPep1-mediated signaling in the roots.
基金This study was supported by grants from the National Natural Science Foundation of China （No. 30672032） and the Excellent Youth Foundation of Anhui Scientific Committee （No. 08040106814）.
文摘Background Preconditioning with remifentanil confers cardioprotection. Since Ca^2＋ overload is a precipitating factor of injury, we determined the effects of remefentanil on intracellular Ca^2＋ （[Ca^2＋]i） and its transients induced by electrical stimulation and caffeine, which reflects Ca^2＋ handling by Ca^2＋ handling proteins, in rat ventricular myocytes. Methods Freshly isolated adult male Sprague-Dawley rat myocytes were loaded with Fura-2/AM and [Ca]i was determined by spectrofluorometry. Remifentanil at 0.1-1000 μg/L was administered. Ten minutes after administration, either 0.2 Hz electrical stimulation was applied or 10 mmol/L caffeine was added. The [Ca^2＋]i, and the amplitude, time resting and 50% decay （t50） of both transients induced by electrical stimulation （E[Ca^2＋]i） and caffeine （C[Ca^2＋]i） were determined. Results Remifentanil （0.1-1000.0 μg/L） decreased the [Ca^2＋]i in a dose-dependent manner. It also decreased the amplitude of both transients dose-dependently. Furthermore, it increased the time to peak and tso of both transients dose-dependently. Conclusion Remifentanil reduced the [Ca^2＋]i and suppressed the transients induced by electrical stimulation and caffeine in rat ventricular myocytes.
