Reciprocal changes in the postnatal expression of the sarcolemmal Na+-Ca2+-exchanger and SERCA2 in rat heart

Vetter, Roland; Studer, Rebecca K.; Reinecke, Hans; Kolář, František; Ošťádalová, I; Drexler, Helmut

doi:10.1016/s0022-2828(95)90788-2

Cited by 83 publications

(36 citation statements)

References 42 publications

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“…ally, the sarcoplasmic reticulum in neonatal cardiomyocytes is poorly developed, and the levels of SERCA2 mRNA and protein expression are also reduced compared with adult cardiomyocytes (34).…”

Section: Discussionmentioning

confidence: 98%

Protein kinase C-α-induced hypertrophy of neonatal rat ventricular myocytes

Vijayan

Szotek

Martin

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Discussionmentioning

confidence: 98%

Protein kinase C-α-induced hypertrophy of neonatal rat ventricular myocytes

Vijayan

Szotek

Martin

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…one of them would be the greater availability of cytosolic Ca 2+ to be taken up by sERCA not only because of the greater Ca 2+ influx but also due to less Ca 2+ extrusion by the nCX, the main sarcolemmal transporter that removes Ca 2+ from the cytosol. This may be particularly important in the neonatal myocardium, where nCX expression is higher and the exchanger plays a greater role in cytosolic Ca 2+ clearance than in the adult [4,27,29]. We estimate that increasing [Ca 2+ ] o to 2 mM would cause a 10 mv negative shift of the nCX reversal potential, which should decrease diastolic Ca 2+ efflux and possibly favor transport in the Ca 2+ influx mode during sarcolemmal depolarization.…”

Section: Discussionmentioning

confidence: 87%

Blood Calcium Levels in Immature Rats: Influence of Extracellular Calcium Concentration on Myocardial Calcium Handling

et al. 2012

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Abstract:Calcium ions play an important role in several cell functions, from fertilization to cell death. from 1.2 to 2 mM, which also increased the Ca 2+ content in the sarcoplasmic reticulum (SR), and changed the pattern of competition between the main transporters that remove Ca 2+ from the cytosol (SR Ca 2+ -ATPase and Na + /Ca 2+ exchanger). These observations stress the importance of using physiological [Ca 2+ ] o values for reliability of results. It is expected that the present calcemia data, reported for the first time in immature rats, may contribute to the refinement of in vitro experiments with neonatal rat preparations.

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“…In neonatal mammalian heart, the SR is poorly developed (Olivetti et al, 1980;Tanaka et al, 1989) and contractility depends mainly on sarcolemmal Ca 2+ influx (Mahony, 1996). Moreover, the NCX also plays a major role in Ca 2+ extrusion in the neonatal myocardium (Artman, 1992;Vetter et al, 1995). Thus, knowledge of the mechanisms responsible for the recovery from acidosis in toad ventricle might also contribute to a better understanding of the behaviour of neonatal mammalian heart during acidosis.…”

Section: +mentioning

confidence: 99%

Contractile recovery from acidosis in toad ventricle is independent of intracellular pH and relies upon Ca2+ influx

Salas

Petroff

Venosa

et al. 2006

Journal of Experimental Biology

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SUMMARY Hypercapnic acidosis produces a negative inotropic effect on myocardial contractility followed by a partial recovery that occurs in spite of the persistent extracellular acidosis. The underlying mechanisms of this recovery are far from understood, especially in those species in which excitation–contraction coupling differs from that of the mammalian heart. The main goal of the present experiments was to obtain a better understanding of these mechanisms in the toad heart. Hypercapnic acidosis,induced by switching from a bicarbonate-buffered solution equilibrated with 5%CO2 to the same solution equilibrated with 12% CO2,evoked a decrease in contractility followed by a recovery that reached values higher than controls after 30 min of continued acidosis. This contractile pattern was associated with an initial decrease in intracellular pH(pHi) that recovered to control values in spite of the persistent extracellular acidosis. Blockade of the Na+/H+ exchanger(NHE) with cariporide (5 μmol l–1) produced a complete inhibition of pHi restitution, without affecting the mechanical recovery. Hypercapnic acidosis also produced a gradual increase of diastolic and peak Ca2+i transient values, which occurred immediately after the acidosis was settled and persisted during the mechanical recovery phase. Inhibition of Ca2+ influx through the reverse mode of the Na+/Ca2+ exchanger (NCX) by KB-R (1 μmol l–1 for myocytes and 20 μmol l–1 for ventricular strips), or of L-type Ca2+ channels by nifedipine (0.5μmol l–1), completely abolished the mechanical recovery. Acidosis also produced an increase in the action potential duration. This prolongation persisted throughout the acidosis period. Our results show that in toad ventricular myocardium, acidosis produces a decrease in contractility,due to a decrease in Ca2+ myofilament responsiveness, followed by a contractile recovery, which is independent of pHi recovery and relies on an increase in the influx of Ca2+. The results further indicate that both the reverse mode NCX and the L-type Ca2+channels, appear to be involved in the increase in intracellular Ca2+ concentration that mediates the contractile recovery from acidosis.

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Reciprocal changes in the postnatal expression of the sarcolemmal Na+-Ca2+-exchanger and SERCA2 in rat heart

Cited by 83 publications

References 42 publications

Protein kinase C-α-induced hypertrophy of neonatal rat ventricular myocytes

Protein kinase C-α-induced hypertrophy of neonatal rat ventricular myocytes

Blood Calcium Levels in Immature Rats: Influence of Extracellular Calcium Concentration on Myocardial Calcium Handling

Contractile recovery from acidosis in toad ventricle is independent of intracellular pH and relies upon Ca2+ influx

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