Defective excitation-contraction coupling in experimental cardiac hypertrophy and heart failure

Science

Volumn 276, Issue 5313, 1997, Pages 800-806

  Gomez A M ^a   Valdivia, H H ^a   Cheng, H ^a   Lederer, Miriam R ^a   Santana, L F ^a   Cannell, M B ^a   McCune, S A ^a   Altschuld, R A ^a   Lederer, W J ^a  

^a NONE

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM CHANNEL; CALCIUM ION;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BETA ADRENERGIC STIMULATION; CALCIUM CURRENT; CONTROLLED STUDY; EXCITATION CONTRACTION COUPLING; HEART ARRHYTHMIA; HEART FAILURE; HEART HYPERTROPHY; HEART MUSCLE CELL; HYPERTENSION; NONHUMAN; PRIORITY JOURNAL; RAT; SARCOPLASMIC RETICULUM;

ADRENERGIC BETA-AGONISTS; ANIMALS; CALCIUM; CALCIUM CHANNEL BLOCKERS; CALCIUM CHANNELS; CALCIUM CHANNELS, L-TYPE; CARDIOMEGALY; CELL MEMBRANE; HEART FAILURE, CONGESTIVE; HYPERTENSION; ISOPROTERENOL; MICROSCOPY, CONFOCAL; MUSCLE PROTEINS; MYOCARDIAL CONTRACTION; MYOCARDIUM; NIFEDIPINE; PATCH-CLAMP TECHNIQUES; RATS; RATS, INBRED STRAINS; RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL; SARCOPLASMIC RETICULUM;

ANIMALIA;

EID: 1842294625     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.276.5313.800     Document Type: Article

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66. M. Esler, in Hypertension: Pathophysiology, Diagnosis and Management, J. H. Laragh and B. M. Brenner, Eds. (Raven, New York, ed. 2, 1995), pp. 755-773; N. Kaplan, in Clinical Hypertension (Williams and Wilkins, Baltimore, MD, 1990), pp. 95-100.
67. Spontaneously hypertensive SH-HF/Mcc-facp (SH-HF) rats have been selectively bred for congestive heart failure, and those carrying the facp (corpulent) gene, which encodes a defective leptin receptor [S. C. Chua Jr. et al., Science 271, 994 (1996)] have an earlier onset of the disease [S. A. McCune, P. B. Baker, H. F. Stills, ILAR News 32, 23 (1990)]. Hearts from failing SH-HF rats exhibit mechanical alterations and the more negative force-frequency relation thought to reflect SR dysfunction in the failing rat myocardium [P. Narayan et al., J. Mol. Cell. Cardiol. 27, 523 (1995)), but SERCA2 protein is not decreased (R. M. Phillips, unpublished observations). Myocytes were isolated from four phenotypically lean 17-to 18-month-old male SH-HF rats heterozygous for the facp gene. Two animals were from the McCune colony at Ohio State University and two were from Genetic Models (Indianapolis, IN). M-Mode echocardiography [G. J. Haas, S. A. McCune, D. M. Brown, R. J. Cody, Am. Heart J. 130, 806 (1995)] under anesthesia (50 mg of ketamine per kilogram of body weight and 10 mg/kg xylazine) indicated that shortening fractions for the SH-HF rats (37 ± 3%) were significantly (P < 0.01) reduced relative to those of three 17-to 18-month-old Sprague-Dawley controls (57 ± 4%). Peak systolic blood pressure for the SH-HF rats was 164 ± 11 mm Hg versus 108 ± 10 mm Hg for the controls (P < 0.02). All of the failing rats had ascites, hydrothorax, and hepatic and pulmonary congestion; three also had large, well-resolved atrial thrombi. None of the controls exhibited these generally accepted signs of congestive heart failure.
68. Spontaneously hypertensive SH-HF/Mcc-facp (SH-HF) rats have been selectively bred for congestive heart failure, and those carrying the facp (corpulent) gene, which encodes a defective leptin receptor [S. C. Chua Jr. et al., Science 271, 994 (1996)] have an earlier onset of the disease [S. A. McCune, P. B. Baker, H. F. Stills, ILAR News 32, 23 (1990)]. Hearts from failing SH-HF rats exhibit mechanical alterations and the more negative force-frequency relation thought to reflect SR dysfunction in the failing rat myocardium [P. Narayan et al., J. Mol. Cell. Cardiol. 27, 523 (1995)), but SERCA2 protein is not decreased (R. M. Phillips, unpublished observations). Myocytes were isolated from four phenotypically lean 17-to 18-month-old male SH-HF rats heterozygous for the facp gene. Two animals were from the McCune colony at Ohio State University and two were from Genetic Models (Indianapolis, IN). M-Mode echocardiography [G. J. Haas, S. A. McCune, D. M. Brown, R. J. Cody, Am. Heart J. 130, 806 (1995)] under anesthesia (50 mg of ketamine per kilogram of body weight and 10 mg/kg xylazine) indicated that shortening fractions for the SH-HF rats (37 ± 3%) were significantly (P < 0.01) reduced relative to those of three 17-to 18-month-old Sprague-Dawley controls (57 ± 4%). Peak systolic blood pressure for the SH-HF rats was 164 ± 11 mm Hg versus 108 ± 10 mm Hg for the controls (P < 0.02). All of the failing rats had ascites, hydrothorax, and hepatic and pulmonary congestion; three also had large, well-resolved atrial thrombi. None of the controls exhibited these generally accepted signs of congestive heart failure.
69. Spontaneously hypertensive SH-HF/Mcc-facp (SH-HF) rats have been selectively bred for congestive heart failure, and those carrying the facp (corpulent) gene, which encodes a defective leptin receptor [S. C. Chua Jr. et al., Science 271, 994 (1996)] have an earlier onset of the disease [S. A. McCune, P. B. Baker, H. F. Stills, ILAR News 32, 23 (1990)]. Hearts from failing SH-HF rats exhibit mechanical alterations and the more negative force-frequency relation thought to reflect SR dysfunction in the failing rat myocardium [P. Narayan et al., J. Mol. Cell. Cardiol. 27, 523 (1995)), but SERCA2 protein is not decreased (R. M. Phillips, unpublished observations). Myocytes were isolated from four phenotypically lean 17-to 18-month-old male SH-HF rats heterozygous for the facp gene. Two animals were from the McCune colony at Ohio State University and two were from Genetic Models (Indianapolis, IN). M-Mode echocardiography [G. J. Haas, S. A. McCune, D. M. Brown, R. J. Cody, Am. Heart J. 130, 806 (1995)] under anesthesia (50 mg of ketamine per kilogram of body weight and 10 mg/kg xylazine) indicated that shortening fractions for the SH-HF rats (37 ± 3%) were significantly (P < 0.01) reduced relative to those of three 17-to 18-month-old Sprague-Dawley controls (57 ± 4%). Peak systolic blood pressure for the SH-HF rats was 164 ± 11 mm Hg versus 108 ± 10 mm Hg for the controls (P < 0.02). All of the failing rats had ascites, hydrothorax, and hepatic and pulmonary congestion; three also had large, well-resolved atrial thrombi. None of the controls exhibited these generally accepted signs of congestive heart failure.
70. Spontaneously hypertensive SH-HF/Mcc-facp (SH-HF) rats have been selectively bred for congestive heart failure, and those carrying the facp (corpulent) gene, which encodes a defective leptin receptor [S. C. Chua Jr. et al., Science 271, 994 (1996)] have an earlier onset of the disease [S. A. McCune, P. B. Baker, H. F. Stills, ILAR News 32, 23 (1990)]. Hearts from failing SH-HF rats exhibit mechanical alterations and the more negative force-frequency relation thought to reflect SR dysfunction in the failing rat myocardium [P. Narayan et al., J. Mol. Cell. Cardiol. 27, 523 (1995)), but SERCA2 protein is not decreased (R. M. Phillips, unpublished observations). Myocytes were isolated from four phenotypically lean 17-to 18-month-old male SH-HF rats heterozygous for the facp gene. Two animals were from the McCune colony at Ohio State University and two were from Genetic Models (Indianapolis, IN). M-Mode echocardiography [G. J. Haas, S. A. McCune, D. M. Brown, R. J. Cody, Am. Heart J. 130, 806 (1995)] under anesthesia (50 mg of ketamine per kilogram of body weight and 10 mg/kg xylazine) indicated that shortening fractions for the SH-HF rats (37 ± 3%) were significantly (P < 0.01) reduced relative to those of three 17-to 18-month-old Sprague-Dawley controls (57 ± 4%). Peak systolic blood pressure for the SH-HF rats was 164 ± 11 mm Hg versus 108 ± 10 mm Hg for the controls (P < 0.02). All of the failing rats had ascites, hydrothorax, and hepatic and pulmonary congestion; three also had large, well-resolved atrial thrombi. None of the controls exhibited these generally accepted signs of congestive heart failure.
71. Spontaneously hypertensive SH-HF/Mcc-facp (SH-HF) rats have been selectively bred for congestive heart failure, and those carrying the facp (corpulent) gene, which encodes a defective leptin receptor [S. C. Chua Jr. et al., Science 271, 994 (1996)] have an earlier onset of the disease [S. A. McCune, P. B. Baker, H. F. Stills, ILAR News 32, 23 (1990)]. Hearts from failing SH-HF rats exhibit mechanical alterations and the more negative force-frequency relation thought to reflect SR dysfunction in the failing rat myocardium [P. Narayan et al., J. Mol. Cell. Cardiol. 27, 523 (1995)), but SERCA2 protein is not decreased (R. M. Phillips, unpublished observations). Myocytes were isolated from four phenotypically lean 17-to 18-month-old male SH-HF rats heterozygous for the facp gene. Two animals were from the McCune colony at Ohio State University and two were from Genetic Models (Indianapolis, IN). M-Mode echocardiography [G. J. Haas, S. A. McCune, D. M. Brown, R. J. Cody, Am. Heart J. 130, 806 (1995)] under anesthesia (50 mg of ketamine per kilogram of body weight and 10 mg/kg xylazine) indicated that shortening fractions for the SH-HF rats (37 ± 3%) were significantly (P < 0.01) reduced relative to those of three 17-to 18-month-old Sprague-Dawley controls (57 ± 4%). Peak systolic blood pressure for the SH-HF rats was 164 ± 11 mm Hg versus 108 ± 10 mm Hg for the controls (P < 0.02). All of the failing rats had ascites, hydrothorax, and hepatic and pulmonary congestion; three also had large, well-resolved atrial thrombi. None of the controls exhibited these generally accepted signs of congestive heart failure.
72. M. R. Bristow et al., Circulation 82, 112 (1990); J.-M. Moalic, D. Charlemagne, P. Mansier, B. Chevalier, B. Swynghedauw, ibid. 87 (suppl. 4), IV21 (1993). See also (1, 25).
73. M. R. Bristow et al., Circulation 82, 112 (1990); J.-M. Moalic, D. Charlemagne, P. Mansier, B. Chevalier, B. Swynghedauw, ibid. 87 (suppl. 4), IV21 (1993). See also (1, 25).
74. F. T. Thandroyen et al., Circ. Res. 69, 810 (1991); C. T. January and H. A. Fozzard, Pharmacol. Rev. 40, 219 (1988); C. Antzelevitch and S. Sicouri, J. Am. Coll. Cardiol. 23, 1 (1994).
75. F. T. Thandroyen et al., Circ. Res. 69, 810 (1991); C. T. January and H. A. Fozzard, Pharmacol. Rev. 40, 219 (1988); C. Antzelevitch and S. Sicouri, J. Am. Coll. Cardiol. 23, 1 (1994).
76. F. T. Thandroyen et al., Circ. Res. 69, 810 (1991); C. T. January and H. A. Fozzard, Pharmacol. Rev. 40, 219 (1988); C. Antzelevitch and S. Sicouri, J. Am. Coll. Cardiol. 23, 1 (1994).
77. 2 is the variance of the baseline fluorescence. The results of both computer and visual spark-counting methods were in close agreement, with differences of less than 10%.
78. SR-enriched vesicles were isolated by differential centrifugation from whole hearts from control and hypertensive rats as described [C. A. Tate et al., J. Biol. Chem. 260, 9618 (1985)].
79. d is the dissociation constant. Protein concentration was determined by the Bradford method.
80. Supported by the Spanish Ministry of Education and Science (A.M.G.), Maryland Heart Association (H.C.), British Heart Foundation and Wellcome Trust (M.B.C.), NIH grants (L.F.S., H.H.V., S.A.M., R.A.A., and W.J.L.), and a Minority Scientist Development Award from the American Heart Association (H.H.V.). We thank C. Soeller for discussion of computer-modeling results; C. F. Neubauer, P. Sander, S. Park, J. Brenner, R. Ringel, J. Hensley, and K. O'Neill for technical support and for rat echocardiography; Hewlett-Packard for echo equipment; S. M. Wang for help in obtaining and maintaining Dahl rats; and J. Hamlyn, B. H. Scribner, D. Siscovick, and M. P. Blaustein for discussions on hypertension and heart failure.