Efficiency of L‐type Ca2+ Current Compared to Reverse Mode Na/Ca Exchange or T‐type Ca2+ Current as Trigger for Ca2+ Release from the Sarcoplasmic Reticulum

Sipido, Karin R.

doi:10.1111/j.1749-6632.1998.tb08299.x

Cited by 15 publications

(10 citation statements)

References 9 publications

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“…However, it is not clear that the exchanger is located sufficiently close to the ryanodine receptors, 5 or that the flux rate of Ca 2ϩ through the exchanger is sufficient to make Ca 2ϩ entry via this pathway an effective trigger under normal conditions. 22,23 This observation could, however, explain why it has proved so difficult to measure an exchange current accompanying putative Na ϩ -Ca 2ϩ exchange-generated Ca 2ϩ release: a small I Na/Ca flowing in the t-tubules might, under some conditions, be sufficient to cause release, because Ca 2ϩ will be delivered close to the ryanodine receptor, but might be difficult to detect. The location of the exchanger may also enable Ca 2ϩ influx via the exchanger to load the SR with Ca 2ϩ , 9 because SR Ca-ATPase is found adjacent to the t-tubules, 24 so that Ca 2ϩ entering the cell via the exchanger may be sequestered by these pumps.…”

Section: Distribution Of the Namentioning

confidence: 95%

Na ⁺ -Ca ²⁺ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Yang

Pascarel

Steele

et al. 2002

Circulation Research

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Detubulation of rat ventricular myocytes has been used to investigate the role of the t-tubules in Ca2+ cycling during excitation-contraction coupling in rat ventricular myocytes. Ca2+ was monitored using fluo-3 and confocal microscopy. In control myocytes, electrical stimulation caused a spatially uniform increase in intracellular [Ca2+] across the cell width. After detubulation, [Ca2+] rose initially at the cell periphery and then propagated into the center of the cell. Application of caffeine to control myocytes resulted in a rapid and uniform increase of intracellular [Ca2+]; the distribution and amplitude of this increase was the same in detubulated myocytes, although its decline was slower. On application of caffeine to control cells, there was a large, rapid, and transient rise in extracellular [Ca2+] as Ca2+ was extruded from the cell; this rise was significantly smaller in detubulated cells, and the remaining increase was blocked by the sarcolemmal Ca2+ ATPase inhibitor carboxyeosin. The treatment used to produce detubulation had no significant effect on Ca2+ efflux in atrial cells, which lack t-tubules. Detubulation of ventricular myocytes also resulted in loss of Na+-Ca2+ exchange current, although the density of the fast Na+ current was unaltered. It is concluded that Na+-Ca2+ exchange function, and hence Ca2+ efflux by this mechanism, is concentrated in the t-tubules, and that the concentration of Ca2+ flux pathways in the t-tubules is important in producing a uniform increase in intracellular Ca2+ on stimulation.

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Section: Distribution Of the Namentioning

confidence: 95%

Na ⁺ -Ca ²⁺ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Yang

Pascarel

Steele

et al. 2002

Circulation Research

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“…Current densities measured with all K ϩ replaced with Cs ϩ were not different from those with K ϩ (1.25Ϯ0.62 versus 1.23Ϯ0.65 pA/pF at ϩ70 mV in each group of 3 cells from the same heart), as previously reported. 18 …”

Section: Solutions and Experimental Protocolsmentioning

confidence: 99%

Enhanced Ca ²⁺ Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes

et al. 2000

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Background-Ventricular arrhythmias are a major cause of sudden death in patients with heart failure and hypertrophy.The dog with chronic complete atrioventricular block (CAVB) has biventricular hypertrophy and ventricular arrhythmias and is a useful model to study underlying cellular mechanisms. We investigated whether changes in Ca 2ϩ homeostasis are part of the contractile adaptation to CAVB and might contribute to arrhythmogenesis. Methods and Results-In enzymatically isolated myocytes, cell shortening, Ca 2ϩ release from the sarcoplasmic reticulum (SR), and SR Ca 2ϩ content were enhanced at low stimulation frequencies. Ca 2ϩ influx through L-type Ca 2ϩ channels was unchanged, but Ca 2ϩ influx via the Na/Ca exchanger was increased and contributed to Ca 2ϩ loading of the SR. Inward Na/Ca exchange currents were also larger. Changes in Ca 2ϩ fluxes were less pronounced in the right versus left ventricle. Conclusions-Enhanced Na/Ca exchange activity may improve contractile adaptation to CAVB but at the same time facilitate arrhythmias by (1) increasing the propensity to Ca 2ϩ overload, (2) providing more inward current leading to (nonhomogeneous) action potential prolongation, and (3)

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“…29 Myocytes were studied under voltage clamp, using the ruptured whole-cell recording technique. 30 Membrane currents were filtered at 2 kHz and sampled and digitized at 4 kHz.…”

Section: Measurements Of [Ca 2؉ ] I and Membrane Currentsmentioning

confidence: 99%

Ca ²⁺ Uptake by the Sarcoplasmic Reticulum in Ventricular Myocytes of the SERCA2 ^b/b Mouse Is Impaired at Higher Ca ²⁺ Loads Only

Antoons

Heyen

Raeymaekers

et al. 2003

Circulation Research

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Abstract-SERCA2a is the cardiac-specific isoform of Ca 2ϩ -ATPase of the sarcoplasmic reticulum (SR). A reduction of SERCA2a has been implicated in the contractile dysfunction of heart failure, and partial knockout of the SERCA2 gene (Atp2a2 ϩ/Ϫ mice) reiterated many of the features of heart failure. Yet, mice with a mutation of Atp2a2, resulting in full suppression of the SERCA2a isoform and expression of the SERCA2b isoform only (SERCA2

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Efficiency of L‐type Ca²⁺ Current Compared to Reverse Mode Na/Ca Exchange or T‐type Ca²⁺ Current as Trigger for Ca²⁺ Release from the Sarcoplasmic Reticulum

Cited by 15 publications

References 9 publications

Na ⁺ -Ca ²⁺ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Na ⁺ -Ca ²⁺ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Enhanced Ca ²⁺ Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes

Ca ²⁺ Uptake by the Sarcoplasmic Reticulum in Ventricular Myocytes of the SERCA2 ^b/b Mouse Is Impaired at Higher Ca ²⁺ Loads Only

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Efficiency of L‐type Ca2+ Current Compared to Reverse Mode Na/Ca Exchange or T‐type Ca2+ Current as Trigger for Ca2+ Release from the Sarcoplasmic Reticulum

Cited by 15 publications

References 9 publications

Na + -Ca 2+ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Na + -Ca 2+ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Enhanced Ca 2+ Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes

Ca 2+ Uptake by the Sarcoplasmic Reticulum in Ventricular Myocytes of the SERCA2 b/b Mouse Is Impaired at Higher Ca 2+ Loads Only

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Efficiency of L‐type Ca²⁺ Current Compared to Reverse Mode Na/Ca Exchange or T‐type Ca²⁺ Current as Trigger for Ca²⁺ Release from the Sarcoplasmic Reticulum

Na ⁺ -Ca ²⁺ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Na ⁺ -Ca ²⁺ Exchange Activity Is Localized in the T-Tubules of Rat Ventricular Myocytes

Enhanced Ca ²⁺ Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes

Ca ²⁺ Uptake by the Sarcoplasmic Reticulum in Ventricular Myocytes of the SERCA2 ^b/b Mouse Is Impaired at Higher Ca ²⁺ Loads Only