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001-es BibID:	BIBFORM001086
Első szerző:	Chen-Izu, Ye
Cím:	Hypertension-induced remodeling of cardiac excitation-contraction coupling in ventricular myocytes occurs prior to hypertrophy development / Chen-Izu Y., Chen L., Bányász T., McCulle S. L., Norton B., Scharf S. M., Agarwal A., Patwardhan A., Izu L. T., Balke C. W.
Dátum:	2007
ISSN:	0363-6135 (Print)
Megjegyzések:	Hypertension is a major risk factor for developing cardiac hypertrophy and heart failure. Previous studies show that hypertrophied and failing hearts display alterations in excitation-contraction (E-C) coupling. However, it is unclear whether remodeling of the E-C coupling system occurs before or after heart disease development. We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. Here we tested this hypothesis by utilizing the progressive development of hypertensive heart disease in the spontaneously hypertensive rat (SHR) to identify a window period when SHR had just developed hypertension but had not yet developed hypertrophy. We found the following major changes in cardiac E-C coupling during this window period. 1) Using echocardiography and hemodynamics measurements, we found a decrease of left ventricular ejection fraction and cardiac output after the onset of hypertension. 2) Studies in isolated ventricular myocytes showed that myocardial contraction was also enhanced at the same time. 3) The action potential became prolonged. 4) The E-C coupling gain was increased. 5) The systolic Ca(2+) transient was augmented. These data show that profound changes in E-C coupling already occur at the onset of hypertension and precede hypertrophy development. Prolonged action potential and increased E-C coupling gain synergistically increase the Ca(2+) transient. Functionally, augmented Ca(2+) transient causes enhancement of myocardial contraction that can partially compensate for the greater workload to maintain cardiac output. The increased Ca(2+) signaling cascade as a molecular mechanism linking hypertension to cardiac hypertrophy development is also discussed.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	American Journal of Physiology. Heart and Circulatory Physiology 293 (2007), p. 3301-3310. -
További szerzők:	Chen, L. Bányász Tamás (1960-) (élettanász) McCulle, S. L. Norton, Byron Scharf, S. M. Agarwal, Anupam Patwardhan, A. Izu, Leighton T. Balke, C. William
Internet cím:	Elektronikus változat DOI
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001-es BibID:	BIBFORM001084
Első szerző:	Chen-Izu, Ye
Cím:	Phosphorylation of RyR2 and shortening of RyR2 cluster spacing in spontaneously hypertensive rat with heart failure / Chen-Izu Y., Ward C. W., Stark W., Bányász T., Sumandea M. P., Balke W., Izu L. T., Wehrens X. H. T.
Dátum:	2007
ISSN:	0363-6135 (Print)
Megjegyzések:	As a critical step toward understanding the role of abnormal intracellular Ca(2+) release via the ryanodine receptor (RyR(2)) during the development of hypertension-induced cardiac hypertrophy and heart failure, this study examines two questions: 1) At what stage, if ever, in the development of hypertrophy and heart failure is RyR(2) hyperphosphorylated at Ser(2808)? 2) Does the spatial distribution of RyR(2) clusters change in failing hearts? Using a newly developed semiquantitative immunohistochemistry method and Western blotting, we measured phosphorylation of RyR(2) at Ser(2808) in the spontaneously hypertensive rat (SHR) at four distinct disease stages. A major finding is that hyperphosphorylation of RyR(2) at Ser(2808) occurred only at late-stage heart failure in SHR, but not in age-matched controls. Furthermore, the spacing between RyR(2) clusters was shortened in failing hearts, as predicted by quantitative model simulation to increase spontaneous Ca(2+) wave generation and arrhythmias.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	American Journal of Physiology. Heart and Circulatory Physiology 293 (2007), p. 2409-2417. -
További szerzők:	Ward, C. W. Stark, W. Bányász Tamás (1960-) (élettanász) Sumandea, M. P. Balke, C. William Izu, Leighton T. Wehrens, X. H. T.
Internet cím:	elektronikus változat DOI
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