Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle.
A decrease of the transient outward potassium current (Ito) has been observed in cardiac hypertrophy and contributes to the altered shape of the action potential (AP) of hypertrophied ventricular myocytes. Since the shape and duration of the ventricular AP are important determinants of the Ca2+ infl...
| Autori principali: | , , , , |
|---|---|
| Natura: | Journal article |
| Lingua: | English |
| Pubblicazione: |
2005
|
| _version_ | 1826301042770313216 |
|---|---|
| author | Volk, T Noble, P Wagner, M Noble, D Ehmke, H |
| author_facet | Volk, T Noble, P Wagner, M Noble, D Ehmke, H |
| author_sort | Volk, T |
| collection | OXFORD |
| description | A decrease of the transient outward potassium current (Ito) has been observed in cardiac hypertrophy and contributes to the altered shape of the action potential (AP) of hypertrophied ventricular myocytes. Since the shape and duration of the ventricular AP are important determinants of the Ca2+ influx during the AP (QCa), we investigated the effect of ascending aortic stenosis (AS) on QCa in endo- and epicardial myocytes of the left ventricular free wall using the AP voltage-clamp technique. In sham-operated animals, QCa was significantly larger in endocardial compared to epicardial myocytes (803 +/- 65 fC pF(-1), n = 27 vs. 167 +/- 32 fC pF(-1), n = 38, P < 0.001). Ascending aortic stenosis significantly increased QCa in epicardial myocytes (368 +/- 54 fC pF(-1), n = 42, P < 0.05), but did not alter QCa in endocardial myocytes (696 +/- 65 fC pF(-1), n = 26). Peak and current-voltage relation of the AP-induced Ca2+ current were unaffected by AS. However, the time course of the current-voltage relation was significantly prolonged in epicardial myocytes of AS animals. Model calculations revealed that the increase in QCa can be ascribed to a prolonged opening of the activation gate, whereas an increase in inactivation prevents an excessive increase in QCa. In conclusion, AS significantly increased AP-induced Ca2+ influx in epicardial but not in endocardial myocytes of the rat left ventricle. |
| first_indexed | 2024-03-07T05:26:22Z |
| format | Journal article |
| id | oxford-uuid:e0b484a3-8954-4440-9b4b-a7f29348a5a7 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T05:26:22Z |
| publishDate | 2005 |
| record_format | dspace |
| spelling | oxford-uuid:e0b484a3-8954-4440-9b4b-a7f29348a5a72022-03-27T09:49:08ZAscending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:e0b484a3-8954-4440-9b4b-a7f29348a5a7EnglishSymplectic Elements at Oxford2005Volk, TNoble, PWagner, MNoble, DEhmke, HA decrease of the transient outward potassium current (Ito) has been observed in cardiac hypertrophy and contributes to the altered shape of the action potential (AP) of hypertrophied ventricular myocytes. Since the shape and duration of the ventricular AP are important determinants of the Ca2+ influx during the AP (QCa), we investigated the effect of ascending aortic stenosis (AS) on QCa in endo- and epicardial myocytes of the left ventricular free wall using the AP voltage-clamp technique. In sham-operated animals, QCa was significantly larger in endocardial compared to epicardial myocytes (803 +/- 65 fC pF(-1), n = 27 vs. 167 +/- 32 fC pF(-1), n = 38, P < 0.001). Ascending aortic stenosis significantly increased QCa in epicardial myocytes (368 +/- 54 fC pF(-1), n = 42, P < 0.05), but did not alter QCa in endocardial myocytes (696 +/- 65 fC pF(-1), n = 26). Peak and current-voltage relation of the AP-induced Ca2+ current were unaffected by AS. However, the time course of the current-voltage relation was significantly prolonged in epicardial myocytes of AS animals. Model calculations revealed that the increase in QCa can be ascribed to a prolonged opening of the activation gate, whereas an increase in inactivation prevents an excessive increase in QCa. In conclusion, AS significantly increased AP-induced Ca2+ influx in epicardial but not in endocardial myocytes of the rat left ventricle. |
| spellingShingle | Volk, T Noble, P Wagner, M Noble, D Ehmke, H Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle. |
| title | Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle. |
| title_full | Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle. |
| title_fullStr | Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle. |
| title_full_unstemmed | Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle. |
| title_short | Ascending aortic stenosis selectively increases action potential-induced Ca2+ influx in epicardial myocytes of the rat left ventricle. |
| title_sort | ascending aortic stenosis selectively increases action potential induced ca2 influx in epicardial myocytes of the rat left ventricle |
| work_keys_str_mv | AT volkt ascendingaorticstenosisselectivelyincreasesactionpotentialinducedca2influxinepicardialmyocytesoftheratleftventricle AT noblep ascendingaorticstenosisselectivelyincreasesactionpotentialinducedca2influxinepicardialmyocytesoftheratleftventricle AT wagnerm ascendingaorticstenosisselectivelyincreasesactionpotentialinducedca2influxinepicardialmyocytesoftheratleftventricle AT nobled ascendingaorticstenosisselectivelyincreasesactionpotentialinducedca2influxinepicardialmyocytesoftheratleftventricle AT ehmkeh ascendingaorticstenosisselectivelyincreasesactionpotentialinducedca2influxinepicardialmyocytesoftheratleftventricle |