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  • 1
    Online Resource
    Online Resource
    Physiological Changes Induced in Cardiac Myocytes by Cytotoxic Lymphocytes: An Autoimmune Model
    Elsevier BV ; 1994
    In:  Journal of Molecular and Cellular Cardiology Vol. 26, No. 3 ( 1994-03), p. 351-360
    Details
    In: Journal of Molecular and Cellular Cardiology, Elsevier BV, Vol. 26, No. 3 ( 1994-03), p. 351-360
    Type of Medium: Online Resource
    ISSN: 0022-2828
    URL: Article
    DOI: 10.1006/jmcc.1994.1044
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1994
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  • 2
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    Simulations of Reduced Conduction Reserve in the Diabetic Rat Heart: Response to Uncoupling and Reduced Excitability
    Springer Science and Business Media LLC ; 2010
    In:  Annals of Biomedical Engineering Vol. 38, No. 4 ( 2010-4), p. 1415-1425
    Details
    In: Annals of Biomedical Engineering, Springer Science and Business Media LLC, Vol. 38, No. 4 ( 2010-4), p. 1415-1425
    Type of Medium: Online Resource
    ISSN: 0090-6964 , 1573-9686
    URL: Article
    DOI: 10.1007/s10439-009-9855-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 1477155-X
    detail.hit.zdb_id: 185984-5
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  • 3
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    Sex differences in the modulation of K + currents in diabetic rat cardiac myocytes
    Wiley ; 2003
    In:  The Journal of Physiology Vol. 550, No. 2 ( 2003-07), p. 401-412
    Details
    In: The Journal of Physiology, Wiley, Vol. 550, No. 2 ( 2003-07), p. 401-412
    Abstract: A transient ( I peak ) and a sustained ( I sus ) outward K + current were measured, using whole‐cell voltage‐clamp methods, in isolated rat ventricular myocytes obtained by enzymatic dispersion. A comparison was made between male and female rats following induction of (insulin‐deficient) diabetes with streptozotocin (STZ). In control (non‐diabetic) rats, both currents were smaller in cells obtained from females, as compared to males ( P 〈 0.005 ). However, whereas inducing diabetes in male rats significantly attenuated both I peak and I sus ( P 〈 0.005 ), I peak was unchanged in female diabetic rats. I sus was significantly ( P 〈 0.005 ) reduced, but the extent of reduction was smaller ( P 〈 0.02 ) than in males. The formation of angiotensin II (ATII) or endothelin‐1 (ET‐1) was blocked using inhibitors of angiotensin‐converting enzyme (ACE) and endothelin‐converting enzyme (ECE), respectively. In cells from diabetic males both inhibitors significantly ( P 〈 0.005 ) enhanced K + currents. In contrast, no effect was observed in cells from female diabetic rats. However, in ovariectomized (Ovx) diabetic females the in vitro inhibition of ATII and ET‐1 formation augmented the two K + currents, but not when oestradiol was administered in vivo prior to cell isolation. In cells from diabetic males, incubation with 100 nM 17β‐oestradiol significantly ( P 〈 0.005 ) enhanced both I peak and I sus . This effect was blocked if ATII or ET‐1 was added to the medium. These results show that autocrine modulation of K + currents by renin‐angiotensin and endothelin systems is attenuated or absent in female diabetic rats. Oestradiol plays a key role in reducing this modulation. These results may underlie some of the sex differences associated with development of cardiac arrhythmias.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Article
    DOI: 10.1113/jphysiol.2003.041269
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 1475290-6
    detail.hit.zdb_id: 3115-X
    SSG: 12
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  • 4
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    Online Resource
    Gender‐dependent attenuation of cardiac potassium currents in type 2 diabetic db/db mice
    Wiley ; 2004
    In:  The Journal of Physiology Vol. 555, No. 2 ( 2004-03), p. 345-354
    Details
    In: The Journal of Physiology, Wiley, Vol. 555, No. 2 ( 2004-03), p. 345-354
    Abstract: Single ventricular myocytes were prepared from control db /+ and insulin‐resistant diabetic db/db male mice at 6 and 12 weeks of age. Peak and sustained outward potassium currents were measured using whole‐cell voltage clamp methods. At 6 weeks currents were fully developed in control and diabetic mice, with no differences in the density of either current. By 12 weeks both currents were significantly attenuated in the diabetic mice, but could be augmented by in vitro incubation with the angiotensin‐converting enzyme (ACE) inhibitor quinapril (1 μ m , 5–9 h). In cells from female db/db mice (12 weeks of age), K + currents were not attenuated and no effects of quinapril were observed. To investigate whether lack of insulin action accounts for these gender differences, cells were also isolated from cardiomyocte‐specific insulin receptor knockout (CIRKO) mice. Both K + currents were significantly attenuated in cells from male and female CIRKO mice, and action potentials were significantly prolonged. Incubation with quinapril did not augment K + currents. Our results demonstrate that type 2 diabetes is associated with gender‐selective attenuation of K + currents in cardiomyocytes, which may underlie gender differences in the development of some cardiac arrhythmias. The mechanism for attenuation of K + currents in cells from male mice is due, at least in part, to an autocrine effect resulting from activation of a cardiac renin–angiotensin system. Insulin is not involved in these gender differences, since the absence of insulin action in CIRKO mice diminishes K + currents in cells from both males and females.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Article
    DOI: 10.1113/jphysiol.2003.055590
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2004
    detail.hit.zdb_id: 1475290-6
    detail.hit.zdb_id: 3115-X
    SSG: 12
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  • 5
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    Gender differences in ANG II levels and action on multiple K + current modulation pathways in diabetic rats
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 287, No. 1 ( 2004-07), p. H311-H319
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 287, No. 1 ( 2004-07), p. H311-H319
    Abstract: Gender differences were studied in ventricular myocytes from insulin-deficient (Type 1) diabetic rats. Cells were obtained by enzymatic dispersion of hearts from control male and female rats and from rats made diabetic with streptozotocin (100 mg/kg) 7–14 days before experiments. ANG II content, measured by ELISA, was augmented in diabetic males but unaltered in diabetic females. In diabetic ovariectomized females, ANG II levels were augmented as in males. ANG II affects multiple cellular pathways including activation of protein kinase C (PKC) and several tyrosine kinases as well as inhibition of protein kinase A (PKA). The involvement of these pathways in modulating outward K + currents was studied. Transient and sustained outward K + currents were measured using the whole cell voltage-clamp method. In males, these currents are attenuated under diabetic conditions but are augmented by the ANG II-converting enzyme inhibitor quinapril. Activation of PKA by 8-bromo-cAMP enhanced both K + currents in cells from diabetic males. The augmentation of these currents by quinapril was blocked when PKA inhibition was maintained with the Rp isomer of 3′,5′-cyclic monophosphorothioate. Inhibition of tyrosine kinases by genistein also augmented K + currents in cells from diabetic males. Action potentials were abbreviated by 8-bromo-cAMP and genistein. However, both genistein and 8-bromo-cAMP had no effect on K + currents in cells from diabetic females. In cells from ovariectomized diabetic females, 8-bromo-cAMP and genistein enhanced these K + currents as in males. Inhibition of PKC augmented the transient and sustained K + currents in cells from diabetic males and females. A contribution of non-ANG II-dependent activation of PKC is suggested. These results describe some of the mechanisms that may underlie gender-specific differences in the development of cardiac disease and arrhythmias.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01212.2003
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 6
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    Differential autocrine modulation of atrial and ventricular potassium currents and of oxidative stress in diabetic rats
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 290, No. 5 ( 2006-05), p. H1879-H1888
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 290, No. 5 ( 2006-05), p. H1879-H1888
    Abstract: The autocrine modulation of cardiac K + currents was compared in ventricular and atrial cells (V and A cells, respectively) from Type 1 diabetic rats. K + currents were measured by using whole cell voltage clamp. ANG II was measured by ELISA and immunofluorescent labeling. Oxidative stress was assessed by immunofluorescent labeling with dihydroethidium, a measure of superoxide ions. In V cells, K + currents are attenuated after activation of the renin-angiotensin system (RAS) and the resulting ANG II-mediated oxidative stress. In striking contrast, these currents are not attenuated in A cells. Inhibition of the angiotensin-converting enzyme (ACE) also has no effect, in contrast to current augmentation in V cells. ANG II levels are enhanced in V, but not in A, cells. However, the high basal ANG II levels in A cells suggest that in these cells, ANG II-mediated pathways are suppressed, rather than ANG II formation. Concordantly, superoxide ion levels are lower in diabetic A than in V cells. Several findings indicate that high atrial natriuretic peptide (ANP) levels in A cells inhibit RAS activation. In male diabetic V cells, in vitro ANP (300 nM–1 μM, 〉 5 h) decreases oxidative stress and augments K + currents, but not when excess ANG II is present. ANP has no effect on ventricular K + currents when the RAS is not activated, as in control males, in diabetic males treated with ACE inhibitor and in diabetic females. In conclusion, the modulation of K + currents and oxidative stress is significantly different in A and V cells in diabetic rat hearts. The evidence suggests that this is largely due to inhibition of RAS activation and/or action by ANP in A cells. These results may underlie chamber-specific arrhythmogenic mechanisms.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01045.2005
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
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    Sex-dependent impairment of cardiac action potential conduction in type 1 diabetic rats
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 296, No. 5 ( 2009-05), p. H1442-H1450
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 296, No. 5 ( 2009-05), p. H1442-H1450
    Abstract: The incidence of diabetes mellitus is increasing. Cardiac dysfunction often develops, resulting in diverse arrhythmias. These arise from ion channel remodeling or from altered speed and pattern of impulse propagation. Few studies have investigated impulse propagation in the diabetic heart. We previously showed a reduced conduction reserve in the diabetic heart, with associated changes in intercellular gap junctions. The present study investigated whether these effects are sex specific. Hearts from control and streptozotocin-diabetic male and female rats were used. Optical mapping was performed with the voltage-sensitive dye di-4-ANEPPS, using Langendorff-perfused hearts. Isolated ventricular cells and tissue sections were used for immunofluorescent labeling of the gap junction protein connexin43 (Cx43). The gap junction uncoupler heptanol (0.75 mM) or elevated K + (9 mM, to reduce cell excitability) produced significantly greater slowing of propagation in diabetic males than females. In ovariectomized diabetic females, 9 mM K + slowed conduction significantly more than in nonovariectomized females. The subcellular redistribution (lateralization) of the gap junction protein Cx43 was smaller in diabetic females. Pretreatment of diabetic males with the angiotensin-converting enzyme inhibitor quinapril reduced Cx43 lateralization and the effects of 9 mM K + on propagation. In conclusion, the slowing of cardiac impulse propagation in type 1 diabetes is smaller in female rats, partly due to the presence of female sex hormones. This difference is (partly) mediated by sex differences in activation of the cardiac renin-angiotensin system.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01150.2008
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    T-2 toxin effect on cultured myocardial cells
    Elsevier BV ; 1986
    In:  Toxicology Letters Vol. 31, No. 1 ( 1986-4), p. 1-8
    Details
    In: Toxicology Letters, Elsevier BV, Vol. 31, No. 1 ( 1986-4), p. 1-8
    Type of Medium: Online Resource
    ISSN: 0378-4274
    URL: Article
    DOI: 10.1016/0378-4274(86)90187-6
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1986
    detail.hit.zdb_id: 433788-8
    SSG: 12
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  • 9
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    Ser-2030, but not Ser-2808, is the major phosphorylation site in cardiac ryanodine receptors responding to protein kinase A activation upon β-adrenergic stimulation in normal and failing hearts
    Portland Press Ltd. ; 2006
    In:  Biochemical Journal Vol. 396, No. 1 ( 2006-05-15), p. 7-16
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 396, No. 1 ( 2006-05-15), p. 7-16
    Abstract: We have recently shown that RyR2 (cardiac ryanodine receptor) is phosphorylated by PKA (protein kinase A/cAMP-dependent protein kinase) at two major sites, Ser-2030 and Ser-2808. In the present study, we examined the properties and physiological relevance of phosphorylation of these two sites. Using site- and phospho-specific antibodies, we demonstrated that Ser-2030 of both recombinant and native RyR2 from a number of species was phosphorylated by PKA, indicating that Ser-2030 is a highly conserved PKA site. Furthermore, we found that the phosphorylation of Ser-2030 responded to isoproterenol (isoprenaline) stimulation in rat cardiac myocytes in a concentration- and time-dependent manner, whereas Ser-2808 was already substantially phosphorylated before β-adrenergic stimulation, and the extent of the increase in Ser-2808 phosphorylation after β-adrenergic stimulation was much less than that for Ser-2030. Interestingly, the isoproterenol-induced phosphorylation of Ser-2030, but not of Ser-2808, was markedly inhibited by PKI, a specific inhibitor of PKA. The basal phosphorylation of Ser-2808 was also insensitive to PKA inhibition. Moreover, Ser-2808, but not Ser-2030, was stoichiometrically phosphorylated by PKG (protein kinase G). In addition, we found no significant phosphorylation of RyR2 at the Ser-2030 PKA site in failing rat hearts. Importantly, isoproterenol stimulation markedly increased the phosphorylation of Ser-2030, but not of Ser-2808, in failing rat hearts. Taken together, these observations indicate that Ser-2030, but not Ser-2808, is the major PKA phosphorylation site in RyR2 responding to PKA activation upon β-adrenergic stimulation in both normal and failing hearts, and that RyR2 is not hyperphosphorylated by PKA in heart failure. Our results also suggest that phosphorylation of RyR2 at Ser-2030 may be an important event associated with altered Ca2+ handling and cardiac arrhythmia that is commonly observed in heart failure upon β-adrenergic stimulation.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/BJ20060116
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2006
    detail.hit.zdb_id: 1473095-9
    detail.hit.zdb_id: 2969-5
    SSG: 12
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  • 10
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    Endogenous ouabain-like compound increases heart muscle contractility
    Springer Science and Business Media LLC ; 1984
    In:  Nature Vol. 307, No. 5949 ( 1984-1), p. 369-371
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 307, No. 5949 ( 1984-1), p. 369-371
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/307369a0
    RVK:
    TA 1000
    RVK:
    UA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1984
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
    SSG: 11
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