-
2
-
-
0023488446
-
Ischemia induces surface membrane dysfunction: mechanism of altered Na+-dependent glucose transport
-
Molitoris B.A., and Kinne R. Ischemia induces surface membrane dysfunction: mechanism of altered Na+-dependent glucose transport. J Clin Invest 80 (1987) 647-654
-
(1987)
J Clin Invest
, vol.80
, pp. 647-654
-
-
Molitoris, B.A.1
Kinne, R.2
-
3
-
-
1342268346
-
Ischemia-induced phosphorylation of phospholemman directly activates rat cardiac Na/K-ATPase
-
This study describes for the first time the phospho-regulation of the cardiac Na/K ATPase by the phosphorylation of phospholemman. In this study, PLM is shown to physically associate with the cardiac Na/K ATPase and PLM phosphorylation mediates stimulation of Na/K pump activity. Cross-linking studies show that the association between the Na/K ATPase α-subunit and PLM is altered by phosphorylation.
-
Fuller W., Eaton P., Bell J.R., and Shattock M.J. Ischemia-induced phosphorylation of phospholemman directly activates rat cardiac Na/K-ATPase. FASEB J 18 (2004) 197-199. This study describes for the first time the phospho-regulation of the cardiac Na/K ATPase by the phosphorylation of phospholemman. In this study, PLM is shown to physically associate with the cardiac Na/K ATPase and PLM phosphorylation mediates stimulation of Na/K pump activity. Cross-linking studies show that the association between the Na/K ATPase α-subunit and PLM is altered by phosphorylation.
-
(2004)
FASEB J
, vol.18
, pp. 197-199
-
-
Fuller, W.1
Eaton, P.2
Bell, J.R.3
Shattock, M.J.4
-
4
-
-
11144302603
-
Serine 68 phosphorylation of phospholemman: acute isoform-specific activation of cardiac Na/K ATPase
-
Silverman B.Z., Fuller W., Eaton P., Deng J., Moorman J.R., Cheung J.Y., James A.F., and Shattock M.J. Serine 68 phosphorylation of phospholemman: acute isoform-specific activation of cardiac Na/K ATPase. Cardiovasc Res 65 (2005) 93-103
-
(2005)
Cardiovasc Res
, vol.65
, pp. 93-103
-
-
Silverman, B.Z.1
Fuller, W.2
Eaton, P.3
Deng, J.4
Moorman, J.R.5
Cheung, J.Y.6
James, A.F.7
Shattock, M.J.8
-
5
-
-
39149133243
-
Phospholemman (FXYD1) is a substrate for multiple protein kinases in vitro
-
2946-Pos
-
Fuller W., and Shattock M.J. Phospholemman (FXYD1) is a substrate for multiple protein kinases in vitro. Biophys J 88 (2005) 2946-Pos
-
(2005)
Biophys J
, vol.88
-
-
Fuller, W.1
Shattock, M.J.2
-
6
-
-
62249137921
-
Na/K ATPase pump current is increased in ventricular myocytes isolated from phospholemman knockout mice
-
Berry R.G., Fuller W., Tucker A.L., and Shattock M.J. Na/K ATPase pump current is increased in ventricular myocytes isolated from phospholemman knockout mice. J Physiol 565P (2005) C171
-
(2005)
J Physiol
, vol.565 P
-
-
Berry, R.G.1
Fuller, W.2
Tucker, A.L.3
Shattock, M.J.4
-
7
-
-
34247603000
-
The intracellular region of FXYD1 is sufficient to regulate cardiac Na/K ATPase
-
Pavlovic D., Fuller W., and Shattock M.J. The intracellular region of FXYD1 is sufficient to regulate cardiac Na/K ATPase. FASEB J 21 (2007) 1539-1546
-
(2007)
FASEB J
, vol.21
, pp. 1539-1546
-
-
Pavlovic, D.1
Fuller, W.2
Shattock, M.J.3
-
8
-
-
34247592229
-
Regulation of cardiac Na/K ATPAse by FXYD1 (phospholemman)
-
Berry R.G., Fuller W., and Shattock M.J. Regulation of cardiac Na/K ATPAse by FXYD1 (phospholemman). J Mol Cell Cardiol 40 (2006) 997A
-
(2006)
J Mol Cell Cardiol
, vol.40
-
-
Berry, R.G.1
Fuller, W.2
Shattock, M.J.3
-
9
-
-
33845607104
-
Phospholemman phosphorylation mediates the protein kinase C-dependent effects on Na+/K+ pump function in cardiac myocytes
-
Han F., Bossuyt J., Despa S., Tucker A.L., and Bers D.M. Phospholemman phosphorylation mediates the protein kinase C-dependent effects on Na+/K+ pump function in cardiac myocytes. Circ Res 99 (2006) 1376-1383
-
(2006)
Circ Res
, vol.99
, pp. 1376-1383
-
-
Han, F.1
Bossuyt, J.2
Despa, S.3
Tucker, A.L.4
Bers, D.M.5
-
10
-
-
0027932798
-
Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of beta-agonist stimulation
-
Luo W., Grupp I.L., Harrer J., Ponniah S., Grupp G., Duffy J.J., Doetschman T., and Kranias E.G. Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of beta-agonist stimulation. Circ Res 75 (1994) 401-409
-
(1994)
Circ Res
, vol.75
, pp. 401-409
-
-
Luo, W.1
Grupp, I.L.2
Harrer, J.3
Ponniah, S.4
Grupp, G.5
Duffy, J.J.6
Doetschman, T.7
Kranias, E.G.8
-
11
-
-
41949138012
-
Phospholemman-mediated activation of Na/K-ATPase limits [Na]i and inotropic state during beta-adrenergic stimulation in mouse ventricular myocytes
-
This reference shows that the rise in intracellular Na induced by a pacing rate increase can be almost completely abrogated by β-adrenoreptor stimulation and this effect is absent in PLM KO mice. Thus demonstrating the physiological role of PLM-to keep intracellular Na low when heart rate increases.
-
Despa S., Tucker A.L., and Bers D.M. Phospholemman-mediated activation of Na/K-ATPase limits [Na]i and inotropic state during beta-adrenergic stimulation in mouse ventricular myocytes. Circulation 117 (2008) 1849-1855. This reference shows that the rise in intracellular Na induced by a pacing rate increase can be almost completely abrogated by β-adrenoreptor stimulation and this effect is absent in PLM KO mice. Thus demonstrating the physiological role of PLM-to keep intracellular Na low when heart rate increases.
-
(2008)
Circulation
, vol.117
, pp. 1849-1855
-
-
Despa, S.1
Tucker, A.L.2
Bers, D.M.3
-
12
-
-
3242679707
-
Threonine-17 phosphorylation of phospholamban: a key determinant of frequency-dependent increase of cardiac contractility
-
Zhao W., Uehara Y., Chu G., Song Q., Qian J., Young K., and Kranias E.G. Threonine-17 phosphorylation of phospholamban: a key determinant of frequency-dependent increase of cardiac contractility. J Mol Cell Cardiol 37 (2004) 607-612
-
(2004)
J Mol Cell Cardiol
, vol.37
, pp. 607-612
-
-
Zhao, W.1
Uehara, Y.2
Chu, G.3
Song, Q.4
Qian, J.5
Young, K.6
Kranias, E.G.7
-
13
-
-
2942741159
-
Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?
-
Sears C.E., Ashley E.A., and Casadei B. Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?. Philos Trans R Soc Lond B Biol Sci 359 (2004) 1021-1044
-
(2004)
Philos Trans R Soc Lond B Biol Sci
, vol.359
, pp. 1021-1044
-
-
Sears, C.E.1
Ashley, E.A.2
Casadei, B.3
-
14
-
-
0038165407
-
Nitric oxide regulation of myocardial contractility and calcium cycling: independent impact of neuronal and endothelial nitric oxide synthases
-
Khan S.A., Skaf M.W., Harrison R.W., Lee K., Minhas K.M., Kumar A., Fradley M., Shoukas A.A., Berkowitz D.E., and Hare J.M. Nitric oxide regulation of myocardial contractility and calcium cycling: independent impact of neuronal and endothelial nitric oxide synthases. Circ Res 92 (2003) 1322-1329
-
(2003)
Circ Res
, vol.92
, pp. 1322-1329
-
-
Khan, S.A.1
Skaf, M.W.2
Harrison, R.W.3
Lee, K.4
Minhas, K.M.5
Kumar, A.6
Fradley, M.7
Shoukas, A.A.8
Berkowitz, D.E.9
Hare, J.M.10
-
15
-
-
13844271328
-
Frequency-dependent acceleration of relaxation in mammalian heart: a property not relying on phospholamban and SERCA2a phosphorylation
-
Valverde C.A., Mundina-Weilenmann C., Said M., Ferrero P., Vittone L., Salas M., Palomeque J., Petroff M.V., and Mattiazzi A. Frequency-dependent acceleration of relaxation in mammalian heart: a property not relying on phospholamban and SERCA2a phosphorylation. J Physiol 562 (2005) 801-813
-
(2005)
J Physiol
, vol.562
, pp. 801-813
-
-
Valverde, C.A.1
Mundina-Weilenmann, C.2
Said, M.3
Ferrero, P.4
Vittone, L.5
Salas, M.6
Palomeque, J.7
Petroff, M.V.8
Mattiazzi, A.9
-
16
-
-
21344446142
-
The nitric oxide donor sodium nitroprusside stimulates the Na+-K+ pump in isolated rabbit cardiac myocytes
-
William M., Vien J., Hamilton E., Garcia A., Bundgaard H., Clarke R.J., and Rasmussen H.H. The nitric oxide donor sodium nitroprusside stimulates the Na+-K+ pump in isolated rabbit cardiac myocytes. J Physiol 565 (2005) 815-825
-
(2005)
J Physiol
, vol.565
, pp. 815-825
-
-
William, M.1
Vien, J.2
Hamilton, E.3
Garcia, A.4
Bundgaard, H.5
Clarke, R.J.6
Rasmussen, H.H.7
-
17
-
-
33751002286
-
β3-receptors mediate adrenergic stimulation of the sarcolemmal Na-K pump
-
Bundgaard H., Garcia A., Hamilton E.J., White C.N., and Rasmussen H.H. β3-receptors mediate adrenergic stimulation of the sarcolemmal Na-K pump. Biophys J 90 (2006) 556A
-
(2006)
Biophys J
, vol.90
-
-
Bundgaard, H.1
Garcia, A.2
Hamilton, E.J.3
White, C.N.4
Rasmussen, H.H.5
-
18
-
-
33750989613
-
Beta(3)-adrenoceptor agonist stimulation of the Na(+), K(+)-pump in rat skeletal muscle is mediated by beta(2)- rather than beta(3)-adrenoceptors
-
Murphy K.T., Bundgaard H., and Clausen T. Beta(3)-adrenoceptor agonist stimulation of the Na(+), K(+)-pump in rat skeletal muscle is mediated by beta(2)- rather than beta(3)-adrenoceptors. Br J Pharmacol 149 (2006) 635-646
-
(2006)
Br J Pharmacol
, vol.149
, pp. 635-646
-
-
Murphy, K.T.1
Bundgaard, H.2
Clausen, T.3
-
19
-
-
0024432514
-
Role of intracellular Na in Ca overload and depressed recovery of ventricular function of reperfused ischemic rat hearts
-
This is a classic paper showing that intracellular Na overload is a key determinant of cell injury in ischaemia and reperfusion.
-
Tani M., and Neely J.R. Role of intracellular Na in Ca overload and depressed recovery of ventricular function of reperfused ischemic rat hearts. Circ Res 65 (1989) 1045-1056. This is a classic paper showing that intracellular Na overload is a key determinant of cell injury in ischaemia and reperfusion.
-
(1989)
Circ Res
, vol.65
, pp. 1045-1056
-
-
Tani, M.1
Neely, J.R.2
-
20
-
-
0026776340
-
23Na-nuclear magnetic resonance study of the isolated rat heart
-
•], highlights the importance of Na overload as a determinant of tissue injury in ischaemia and reperfusion. This paper makes the additional observation that Na overload is a key determinant of electrical dysfunction.
-
•], highlights the importance of Na overload as a determinant of tissue injury in ischaemia and reperfusion. This paper makes the additional observation that Na overload is a key determinant of electrical dysfunction.
-
(1992)
Circulation
, vol.86
, pp. 302-310
-
-
Neubauer, S.1
Newell, J.B.2
Ingwall, J.S.3
-
21
-
-
0037377081
-
Intracellular Na in animal models of hypertrophy and heart failure: contractile function and arrhythmogenesis
-
Pogwizd S.M., Sipido K.R., Verdonck F., and Bers D.M. Intracellular Na in animal models of hypertrophy and heart failure: contractile function and arrhythmogenesis. Cardiovasc Res 57 (2003) 887-896
-
(2003)
Cardiovasc Res
, vol.57
, pp. 887-896
-
-
Pogwizd, S.M.1
Sipido, K.R.2
Verdonck, F.3
Bers, D.M.4
-
23
-
-
0344176432
-
Intracellular sodium concentration and accumulation during ischemia in isolated perfused rat and guinea pig hearts
-
Bernard M., and Ingwall J. Intracellular sodium concentration and accumulation during ischemia in isolated perfused rat and guinea pig hearts. J Mol Cell Cardiol 23 (1991) S8
-
(1991)
J Mol Cell Cardiol
, vol.23
-
-
Bernard, M.1
Ingwall, J.2
-
25
-
-
0025654335
-
Na-NMR measurements of intracellular sodium in intact perfused ferret hearts during ischemia and reperfusion
-
23Na NMR spectroscopy (still the 'gold standard' technique for measuring intracellular Na in intact beating hearts) to measure intracellular Na changes during real (not simulated) ischaemia and reperfusion. This reference (at hypothermic temperatures) and reference [24] (at normothermic temperatures) show that ischaemia causes intracellular Na to rise immediately increasing steadily to 25-30 mM. Importantly, neither of the studies cited here (nor later studies from the van Echteld group with better (<5 s) temporal resolution) could show evidence for the previously hypothesised increase in intracellular Na in the early seconds of reperfusion.
-
23Na NMR spectroscopy (still the 'gold standard' technique for measuring intracellular Na in intact beating hearts) to measure intracellular Na changes during real (not simulated) ischaemia and reperfusion. This reference (at hypothermic temperatures) and reference [24] (at normothermic temperatures) show that ischaemia causes intracellular Na to rise immediately increasing steadily to 25-30 mM. Importantly, neither of the studies cited here (nor later studies from the van Echteld group with better (<5 s) temporal resolution) could show evidence for the previously hypothesised increase in intracellular Na in the early seconds of reperfusion.
-
(1990)
Am J Physiol
, vol.259
-
-
Pike, M.M.1
Kitakaze, M.2
Marban, E.3
-
26
-
-
41549102140
-
Mechanism of action of the new anti-ischemia drug ranolazine
-
Hasenfuss G., and Maier L.S. Mechanism of action of the new anti-ischemia drug ranolazine. Clin Res Cardiol 97 (2008) 222-226
-
(2008)
Clin Res Cardiol
, vol.97
, pp. 222-226
-
-
Hasenfuss, G.1
Maier, L.S.2
-
27
-
-
0023280509
-
Myocardial contractile function during ischemia and hypoxia
-
Allen D.G., and Orchard C.H. Myocardial contractile function during ischemia and hypoxia. Circ Res 60 (1987) 153-168
-
(1987)
Circ Res
, vol.60
, pp. 153-168
-
-
Allen, D.G.1
Orchard, C.H.2
-
29
-
-
0037214918
-
Intracellular Na+ and altered Na+ transport mechanisms in cardiac hypertrophy and failure
-
Verdonck F., Volders P.G., Vos M.A., and Sipido K.R. Intracellular Na+ and altered Na+ transport mechanisms in cardiac hypertrophy and failure. J Mol Cell Cardiol 35 (2003) 5-25
-
(2003)
J Mol Cell Cardiol
, vol.35
, pp. 5-25
-
-
Verdonck, F.1
Volders, P.G.2
Vos, M.A.3
Sipido, K.R.4
-
30
-
-
0037162348
-
Rate dependence of [Na+]i and contractility in nonfailing and failing human myocardium
-
This paper is one of many studies demonstrating that intracellular Na is high in the failing myocardium. In this study, they show that this high Na, at low rates of stimulation, may maintain contractility. However, since this study uses electrical pacing, rather than β-receptor stimulation, it does not provide insight into the role of PLM in regulating Na at physiologically induced (i.e. by catecholamines) high heart rates.
-
Pieske B., Maier L.S., Piacentino III V., Weisser J., Hasenfuss G., and Houser S. Rate dependence of [Na+]i and contractility in nonfailing and failing human myocardium. Circulation 106 (2002) 447-453. This paper is one of many studies demonstrating that intracellular Na is high in the failing myocardium. In this study, they show that this high Na, at low rates of stimulation, may maintain contractility. However, since this study uses electrical pacing, rather than β-receptor stimulation, it does not provide insight into the role of PLM in regulating Na at physiologically induced (i.e. by catecholamines) high heart rates.
-
(2002)
Circulation
, vol.106
, pp. 447-453
-
-
Pieske, B.1
Maier, L.S.2
Piacentino III, V.3
Weisser, J.4
Hasenfuss, G.5
Houser, S.6
-
31
-
-
0037188622
-
Intracellular Na(+) concentration is elevated in heart failure but Na/K pump function is unchanged
-
Despa S., Islam M.A., Weber C.R., Pogwizd S.M., and Bers D.M. Intracellular Na(+) concentration is elevated in heart failure but Na/K pump function is unchanged. Circulation 105 (2002) 2543-2548
-
(2002)
Circulation
, vol.105
, pp. 2543-2548
-
-
Despa, S.1
Islam, M.A.2
Weber, C.R.3
Pogwizd, S.M.4
Bers, D.M.5
-
32
-
-
0037376127
-
Increased Na+ concentration and altered Na/K pump activity in hypertrophied canine ventricular cells
-
Verdonck F., Volders P.G., Vos M.A., and Sipido K.R. Increased Na+ concentration and altered Na/K pump activity in hypertrophied canine ventricular cells. Cardiovasc Res 57 (2003) 1035-1043
-
(2003)
Cardiovasc Res
, vol.57
, pp. 1035-1043
-
-
Verdonck, F.1
Volders, P.G.2
Vos, M.A.3
Sipido, K.R.4
-
33
-
-
0024559253
-
Rat vs. rabbit ventricle: Ca flux and intracellular Na assessed by ion-selective microelectrodes
-
Shattock M.J., and Bers D.M. Rat vs. rabbit ventricle: Ca flux and intracellular Na assessed by ion-selective microelectrodes. Am J Physiol 256 (1989) C813-C822
-
(1989)
Am J Physiol
, vol.256
-
-
Shattock, M.J.1
Bers, D.M.2
-
34
-
-
62249207427
-
Characterisation of the Langendorff-perfused phospholemman knockout mouse heart: effects of calcium concentration and pacing rate on contractility
-
Kennington E., Fuller W., and Shattock M.J. Characterisation of the Langendorff-perfused phospholemman knockout mouse heart: effects of calcium concentration and pacing rate on contractility. J Mol Cell Cardiol 40 (2006) 209
-
(2006)
J Mol Cell Cardiol
, vol.40
, pp. 209
-
-
Kennington, E.1
Fuller, W.2
Shattock, M.J.3
-
35
-
-
0007436490
-
Why does the myocardium fail? Insights from basic science
-
SI8-14
-
Bristow M.R. Why does the myocardium fail? Insights from basic science. Lancet 352 Suppl. 1 (1998) SI8-14
-
(1998)
Lancet
, vol.352
, Issue.SUPPL. 1
-
-
Bristow, M.R.1
-
36
-
-
0019982539
-
Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts
-
Bristow M.R., Ginsburg R., Minobe W., Cubicciotti R.S., Sageman W.S., Lurie K., Billingham M.E., Harrison D.C., and Stinson E.B. Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N Engl J Med 307 (1982) 205-211
-
(1982)
N Engl J Med
, vol.307
, pp. 205-211
-
-
Bristow, M.R.1
Ginsburg, R.2
Minobe, W.3
Cubicciotti, R.S.4
Sageman, W.S.5
Lurie, K.6
Billingham, M.E.7
Harrison, D.C.8
Stinson, E.B.9
-
37
-
-
0030888810
-
Increased expression of cardiac phosphatases in patients with end-stage heart failure
-
Neumann J., Eschenhagen T., Jones L.R., Linck B., Schmitz W., Scholz H., and Zimmermann N. Increased expression of cardiac phosphatases in patients with end-stage heart failure. J Mol Cell Cardiol 29 (1997) 265-272
-
(1997)
J Mol Cell Cardiol
, vol.29
, pp. 265-272
-
-
Neumann, J.1
Eschenhagen, T.2
Jones, L.R.3
Linck, B.4
Schmitz, W.5
Scholz, H.6
Zimmermann, N.7
-
38
-
-
20244377242
-
Enhancement of cardiac function and suppression of heart failure progression by inhibition of protein phosphatase 1
-
Pathak A., del Monte F., Zhao W., Schultz J.E., Lorenz J.N., Bodi I., Weiser D., Hahn H., Carr A.N., Syed F., et al. Enhancement of cardiac function and suppression of heart failure progression by inhibition of protein phosphatase 1. Circ Res 96 (2005) 756-766
-
(2005)
Circ Res
, vol.96
, pp. 756-766
-
-
Pathak, A.1
del Monte, F.2
Zhao, W.3
Schultz, J.E.4
Lorenz, J.N.5
Bodi, I.6
Weiser, D.7
Hahn, H.8
Carr, A.N.9
Syed, F.10
-
39
-
-
0027920980
-
Pathogenetic mechanisms of septic shock
-
Parrillo J.E. Pathogenetic mechanisms of septic shock. N Engl J Med 328 (1993) 1471-1477
-
(1993)
N Engl J Med
, vol.328
, pp. 1471-1477
-
-
Parrillo, J.E.1
-
40
-
-
0031945838
-
Cardiac dysfunction in sepsis: new theories and clinical implications
-
Grocott-Mason R.M., and Shah A.M. Cardiac dysfunction in sepsis: new theories and clinical implications. Intensive Care Med 24 (1998) 286-295
-
(1998)
Intensive Care Med
, vol.24
, pp. 286-295
-
-
Grocott-Mason, R.M.1
Shah, A.M.2
-
41
-
-
62249083339
-
Nitric oxide-induced stimulation of the cardiac Na/K ATPase requires phospholemman
-
Although only in abstract form, this is the first report implicating PLM in the stimulation of the Na/K ATPase by nitric oxide.
-
Hall A.R., McLatchie L.M., Fuller W., and Shattock M.J. Nitric oxide-induced stimulation of the cardiac Na/K ATPase requires phospholemman. J Mol Cell Cardiol 42 6 Suppl. 1 (2007) S54. Although only in abstract form, this is the first report implicating PLM in the stimulation of the Na/K ATPase by nitric oxide.
-
(2007)
J Mol Cell Cardiol
, vol.42
, Issue.6 SUPPL. 1
-
-
Hall, A.R.1
McLatchie, L.M.2
Fuller, W.3
Shattock, M.J.4
-
42
-
-
0038481242
-
Functional modulation of the sodium pump: the regulatory proteins 'Fixit'
-
Cornelius F., and Mahmmoud Y.A. Functional modulation of the sodium pump: the regulatory proteins 'Fixit'. News Physiol Sci 18 (2003) 119-124
-
(2003)
News Physiol Sci
, vol.18
, pp. 119-124
-
-
Cornelius, F.1
Mahmmoud, Y.A.2
-
43
-
-
0041658999
-
Abnormal activation of Na+-K+ pump in aortas from rats with endotoxaemia
-
Chen S.J., Chen K.H., Webb R.C., Yen M.H., and Wu C.C. Abnormal activation of Na+-K+ pump in aortas from rats with endotoxaemia. Naunyn Schmiedebergs Arch Pharmacol 368 (2003) 57-62
-
(2003)
Naunyn Schmiedebergs Arch Pharmacol
, vol.368
, pp. 57-62
-
-
Chen, S.J.1
Chen, K.H.2
Webb, R.C.3
Yen, M.H.4
Wu, C.C.5
-
44
-
-
0028824777
-
Possible role of Na(+)-K(+)-ATPase in the regulation of human corpus cavernosum smooth muscle contractility by nitric oxide
-
Gupta S., Moreland R.B., Munarriz R., Daley J., Goldstein I., and Saenz de Tejada I. Possible role of Na(+)-K(+)-ATPase in the regulation of human corpus cavernosum smooth muscle contractility by nitric oxide. Br J Pharmacol 116 (1995) 2201-2206
-
(1995)
Br J Pharmacol
, vol.116
, pp. 2201-2206
-
-
Gupta, S.1
Moreland, R.B.2
Munarriz, R.3
Daley, J.4
Goldstein, I.5
Saenz de Tejada, I.6
-
45
-
-
49749093088
-
The antianginal agent, ranolazine, reduces myocardial infarct size but does not alter anatomic no-reflow or regional myocardial blood flow in ischemia/reperfusion in the rabbit
-
Hale S.L., and Kloner R.A. The antianginal agent, ranolazine, reduces myocardial infarct size but does not alter anatomic no-reflow or regional myocardial blood flow in ischemia/reperfusion in the rabbit. J Cardiovasc Pharmacol Ther 13 (2008) 226-232
-
(2008)
J Cardiovasc Pharmacol Ther
, vol.13
, pp. 226-232
-
-
Hale, S.L.1
Kloner, R.A.2
-
46
-
-
34247526904
-
Effects of ranolazine on recurrent cardiovascular events in patients with non-ST-elevation acute coronary syndromes: the MERLIN-TIMI 36 randomized trial
-
This is the first report of a clinical trial investigating the effects of a drug suggested to block Na influx into the myocardium in angina. The study shows evidence for protection against arrhythmias.
-
Morrow D.A., Scirica B.M., Karwatowska-Prokopczuk E., Murphy S.A., Budaj A., Varshavsky S., Wolff A.A., Skene A., McCabe C.H., and Braunwald E. Effects of ranolazine on recurrent cardiovascular events in patients with non-ST-elevation acute coronary syndromes: the MERLIN-TIMI 36 randomized trial. JAMA 297 (2007) 1775-1783. This is the first report of a clinical trial investigating the effects of a drug suggested to block Na influx into the myocardium in angina. The study shows evidence for protection against arrhythmias.
-
(2007)
JAMA
, vol.297
, pp. 1775-1783
-
-
Morrow, D.A.1
Scirica, B.M.2
Karwatowska-Prokopczuk, E.3
Murphy, S.A.4
Budaj, A.5
Varshavsky, S.6
Wolff, A.A.7
Skene, A.8
McCabe, C.H.9
Braunwald, E.10
-
47
-
-
0033537359
-
2+-exchanger protein levels and diastolic function of failing human myocardium
-
2+-exchanger protein levels and diastolic function of failing human myocardium. Circulation 99 (1999) 641-648
-
(1999)
Circulation
, vol.99
, pp. 641-648
-
-
Hasenfuss, G.1
Schillinger, W.2
Lehnart, S.E.3
Preuss, M.4
Pieske, B.5
Maier, L.S.6
Prestle, J.7
Minami, K.8
Just, H.9
-
48
-
-
39149126357
-
Don't flog the heart!-development of specific drug therapies for heart failure
-
Rasmussen H.H., and Figtree G. Don't flog the heart!-development of specific drug therapies for heart failure. Crit Care Resusc 9 (2007) 364-369
-
(2007)
Crit Care Resusc
, vol.9
, pp. 364-369
-
-
Rasmussen, H.H.1
Figtree, G.2
-
49
-
-
33947171594
-
NMR of membrane proteins in micelles and bilayers: the FXYD family proteins
-
Franzin C.M., Gong X.M., Thai K., Yu J., and Marassi F.M. NMR of membrane proteins in micelles and bilayers: the FXYD family proteins. Methods 41 (2007) 398-408
-
(2007)
Methods
, vol.41
, pp. 398-408
-
-
Franzin, C.M.1
Gong, X.M.2
Thai, K.3
Yu, J.4
Marassi, F.M.5
-
50
-
-
34250176566
-
Structure of the Na, K-ATPase regulatory protein FXYD1 in micelles
-
Teriete P., Franzin C.M., Choi J., and Marassi F.M. Structure of the Na, K-ATPase regulatory protein FXYD1 in micelles. Biochemistry 46 (2007) 6774-6783
-
(2007)
Biochemistry
, vol.46
, pp. 6774-6783
-
-
Teriete, P.1
Franzin, C.M.2
Choi, J.3
Marassi, F.M.4
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