Calcium currents of isolated bovine ventricular myocytes are fast and of large amplitude

Isenberg, Gerrit; Klöckner, Udo

doi:10.1007/bf00584965

Cited by 272 publications

(133 citation statements)

References 42 publications

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“…Because Na channels would be inactivated by the midplateau phase, the only remaining current would flow through L-type channels. Over the time course of a few milliseconds, activation gating of this channel would equilibrate rapidly with changes in voltage (40), whereas CDI would appear nearly stationary (Fig. 1C Top).…”

Section: Discussionmentioning

confidence: 99%

Engineered calmodulins reveal the unexpected eminence of Ca ²⁺ channel inactivation in controlling heart excitation

Alseikhan

DeMaria

Colecraft

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

179

184

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Section: Discussionmentioning

confidence: 99%

Engineered calmodulins reveal the unexpected eminence of Ca ²⁺ channel inactivation in controlling heart excitation

Alseikhan

DeMaria

Colecraft

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

179

184

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“…The cross-sectional area of the cell was measured with the image-analysis program NIH (National Institutes of Health) Image. The surface area of the cell was then calculated from its cross-sectional area, assuming a spindle shape (surface area =3.14Xcross sectional area) (16).…”

Section: Morphometric Methodsmentioning

confidence: 99%

Voltage-Dependent Ca2+ Channels in Resistance Arteries from Dahl Salt-Sensitive Rats.

et al. 2000

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To determine whether chronic salt-loading would alter voltage-dependent Ca2+ channels in resistance arteries of Dahl salt-sensitive rats, whole-cell voltage-clamp experiments were performed on single cells that were isolated from small mesenteric arteries. Dahl salt-sensitive rats were fed either an 8% NaCI diet (high-NaCI group) or a 0.3% NaCI diet (low-NaCI group) from the age of 6 or 7 weeks. After 4 to 5 weeks, systolic blood pressure was significantly higher in the high-NaCI group than in the low-NaCI group. In the high-NaCI group, the threshold potential for Ca2+ channel current was more negative and the current amplitude that was normalized by cell capacitance was higher at negative command potentials (-40 mV to -20 mV), as compared with the low-NaCI group. When the current was separated into fast transient current and slow sustained (L-type) current, the alteration in the high-NaCI group was attributable to the change in L-type current. The steady-state inactivation curve was not different between the high-NaCI and low-NaCI groups. In conclusion, L-type Ca2+ channels in resistance arteries of Dahl salt-sensitive rats became more available for opening near the resting potential after dietary salt-loading.(Hypertens Res 2000; 23: 701-707)

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“…9 Details of the transport solution and disaggregation have been described. 10 Disaggregated cells were kept in KB medium 11 at room temperature for Ն1 hour before electrophysiological experiments.…”

Section: Isolated Tissue and Single Myocyte Studiesmentioning

confidence: 99%

Transient Outward Current, I _to1 , Is Altered in Cardiac Memory

et al. 1999

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Background-Cardiac memory refers to an altered T-wave morphology induced by ventricular pacing or arrhythmias that persist for variable intervals after resumption of sinus rhythm. Methods and Results-We induced long-term cardiac memory (LTM) in conscious dogs by pacing the ventricles at 120 bpm for 3 weeks. ECGs were recorded daily for 1 hour, during which time pacing was discontinued. At terminal study, the heart was removed and the electrophysiology of left ventricular epicardial myocytes was investigated. Control (C) and LTM ECG did not differ, except for T-wave amplitude, which decreased from 0.12Ϯ0.18 to Ϫ0.34Ϯ0.21 mV (ϮSEM, PϽ0.05), and T-wave vector, which shifted from Ϫ37Ϯ12°to Ϫ143Ϯ4°(PϽ0.05). Epicardial action potentials revealed loss of the notch and lengthening of duration at 20 days (both PϽ0.05). Calcium-insensitive transient outward current (I to ) was investigated by whole-cell patch clamp. No difference in capacitance was seen in C and LTM myocytes. I to activated on membrane depolarization to Ϫ25Ϯ1 mV in C and Ϫ7Ϯ1 mV (PϽ0.05) in LTM myocytes, indicating a positive voltage shift of activation. I to density was reduced in LTM myocytes, and a decreased mRNA level for Kv4.3 was observed. Recovery of I to from inactivation was significantly prolonged: it was 531Ϯ80 ms (nϭ10) in LTM and 27Ϯ6 ms (nϭ9) in C (PϽ0.05) at Ϫ65 mV. Conclusions-I to changes are associated with and can provide at least a partial explanation for action-potential and T-wave changes occurring with LTM. (Circulation. 1999;99:1898-1905.)

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Calcium currents of isolated bovine ventricular myocytes are fast and of large amplitude

Cited by 272 publications

References 42 publications

Engineered calmodulins reveal the unexpected eminence of Ca ²⁺ channel inactivation in controlling heart excitation

Engineered calmodulins reveal the unexpected eminence of Ca ²⁺ channel inactivation in controlling heart excitation

Voltage-Dependent Ca2+ Channels in Resistance Arteries from Dahl Salt-Sensitive Rats.

Transient Outward Current, I _to1 , Is Altered in Cardiac Memory

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Calcium currents of isolated bovine ventricular myocytes are fast and of large amplitude

Cited by 272 publications

References 42 publications

Engineered calmodulins reveal the unexpected eminence of Ca 2+ channel inactivation in controlling heart excitation

Engineered calmodulins reveal the unexpected eminence of Ca 2+ channel inactivation in controlling heart excitation

Voltage-Dependent Ca2+ Channels in Resistance Arteries from Dahl Salt-Sensitive Rats.

Transient Outward Current, I to1 , Is Altered in Cardiac Memory

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Engineered calmodulins reveal the unexpected eminence of Ca ²⁺ channel inactivation in controlling heart excitation

Engineered calmodulins reveal the unexpected eminence of Ca ²⁺ channel inactivation in controlling heart excitation

Transient Outward Current, I _to1 , Is Altered in Cardiac Memory