Rat cardiac hypertrophy Altered sodium‐calcium exchange activity in sarcolemmal vesicles

Hanf, R.; Drubaix, Isabelle; Marotte, F.; Lelièvre, L.

doi:10.1016/0014-5793(88)80303-x

Cited by 60 publications

(10 citation statements)

References 13 publications

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“…Regarding the sarcolemmal Na+/Ca 2+ exchanger, the resuits from the literature are somewhat controversial. In rat models of aortic constriction [68] and myocardial infarction [69], reduced exchanger activity in sarcolemmal preparations has been reported, whereas a recent study measuring membrane currents indicated an enhanced activity in the cardiomyopathic hamster [70]. Consistent with the latter observation, Kent and coworkers [71] showed an increased expression of the Na+/Ca 2+ exchanger gene in an acute right ventricular pressure overload model of the cat.…”

Section: Gene Expression and Function Of Ca 2* Transport Proteins In mentioning

confidence: 73%

Calcium transport proteins in the nonfailing and failing heart: gene expression and function

Wankerl

Schwartz

1995

J Mol Med

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In heart failure alterations of intracellular Ca2+ handling are thought to be a major reason for impaired contraction and relaxation. Peak Ca2+ transients are reduced, resting Ca2+ levels elevated, and the time course of diastolic Ca2+ decline is markedly prolonged in failing hearts. The proteins of the sarcoplasmic reticulum and the sarcolemmal Na+/Ca2+ exchanger are the most important tools for Ca2+ homeostasis in the cardiomyocyte, and their molecular cloning has allowed prediction of structure/function analysis. The investigation of function and gene expression of these proteins in failing myocardium has been an area of intensive research in recent years in order to provide a more detailed understanding of the pathophysiology of heart failure. Quantitative changes in expression of the sarcoplasmic reticulum Ca(2+)-ATPase, the ryanodine receptor, and the Na+/Ca2+ exchanger with correlations to functional alterations have been reported both in experimental animal models and in the human failing heart. However, in human heart failure these findings are currently the subject of a lively discussion because observations have apparently been in part contradictory. This review discusses the proteins involved in myocardial Ca2+ handling and describes the current state of research on expressional and functional alterations and their potential implication in the pathomechanism of heart failure.

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Section: Gene Expression and Function Of Ca 2* Transport Proteins In mentioning

confidence: 73%

Calcium transport proteins in the nonfailing and failing heart: gene expression and function

Wankerl

Schwartz

1995

J Mol Med

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“…Instead, the effects of angiotensin II on cardiac performance (34,51,53,54) and on growth (16,17) appear to be associated with the activation of phosphoinositide second messengers (55-57) and changes in the mobilization and reuptake of cytosolic [Ca2+]i. Cardiac [Ca2+]i homeostasis, which is a major determinant of diastolic function, is profoundly altered in hypertrophied rat myocytes (57)(58)(59), and there is evidence that IP3-induced sarcoplasmic reticulum Ca2' release is enhanced (60). We postulate that the deterioration of diastolic function induced by angiotensin II activation that we observed may be related to the effects of phosphoinositide second messengers on the slowed [Ca2+]i reuptake which is characteristic of hypertrophied myocytes.…”

Section: Discussionmentioning

confidence: 99%

Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation.

Schunkert¹,

Dzau²,

Tang³

et al. 1990

J. Clin. Invest.

589

239

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We compared the activity and physiologic effects of cardiac angiotensin converting enzyme (ACE) using isovolumic hearts from male Wistar rats with left ventricular hypertrophy due to chronic experimental aortic stenosis and from control rats. In response to the infusion of 3.5 X 10-8 M angiotensin I in the isolated buffer perfused beating hearts, the intracardiac fractional conversion to angiotensin II was higher in the hypertrophied hearts compared with the controls (17.3±4.1% vs 6.8±1.3%, P < 0.01). ACE activity was also significantly increased in the free wall, septum, and apex of the hypertrophied left ventricle, whereas ACE activity from the nonhypertrophied right ventricle of the aortic stenosis rats was not different from that of the control rats. Northern blot analyses of poly(A)+ purified RNA demonstrated the expression of ACE mRNA, which was increased fourfold in left ventricular tissue obtained from the hearts with left ventricular hypertrophy compared with the controls. In both groups, the intracardiac conversion of angiotensin I to angiotensin II caused a comparable dose-dependent increase in coronary resistance. In the control hearts, angiotensin II activation had no significant effect on systolic or diastolic function; however, it was associated with a dose-dependent depression of left ventricular diastolic relaxation in the hypertrophied hearts. These novel observations suggest that cardiac ACE is induced in hearts with left ventricular hypertrophy, and that the resultant intracardiac activation of angiotensin II may have differential effects on myocardial relaxation in hypertrophied hearts relative to controls. (J. Clin.

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“…Both diastolic and peak systolic [Ca 2+ ]j increased in a statistically significant manner when perfusion pressure was raised from 80 to 120 mm Hg. The contractile pressure developed by the heart was also augmented in response to the increase in coronary pressure (see 44 and calcium release from the sarcoplasmic reticulum 4546 have been reported to be altered in hypertrophied myocardium, but it is not known whether such changes occur acutely in response to elevated perfusion pressure. Nevertheless, our results do make it clear that the increase in aortic pressure itself suffices to induce an increase in [Ca 2+ ]i.…”

Section: Induction Of Oncogenes By An Increase In Aortic Pressurementioning

confidence: 99%

Cell calcium, oncogenes, and hypertrophy.

Marbán

Koretsune

1990

Hypertension

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Rat cardiac hypertrophy Altered sodium‐calcium exchange activity in sarcolemmal vesicles

Cited by 60 publications

References 13 publications

Calcium transport proteins in the nonfailing and failing heart: gene expression and function

Calcium transport proteins in the nonfailing and failing heart: gene expression and function

Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation.

Cell calcium, oncogenes, and hypertrophy.

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