| Autor: |
Kirstein, Michael, Katzer, Astrid, Kai Hu, Gaudron, Peter, Ertl, Georg, Langenfeld, Heiner, Kochsiek, Kurt |
| Předmět: |
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| Zdroj: |
Pacing & Clinical Electrophysiology; Nov1996, Vol. 19 Issue 11, p2018-2022, 5p |
| Abstrakt: |
There are several reports of an altered β-adrenergic pathway in heart failure. Since the fast cardiac sodium current (INa+ >) is also subject to β-receptor dependent regulation, we investigated its regulation in a model of cardiac dysfunction. Adenylyl cyclase was stimulated directly with forskolin as one step in the β-adrenergic pathway. Twelve-week-old Wistar rats were infarcted by ligation of the left anterior descending coronary artery. Eight weeks later, the induced hemodynamic changes were evaluated. The left ventricular end-diastolic pressure (LVEDP) was used as a measure of the hemodynamic effects of the myocardial infarction. With the loose patch clamp technique, INa+ was measured in intact papillary muscles at an external sodium concentration of 150 mmol/L. Potential dependent availability was tested with pulses to 0 mV from various conditioning potentials. In animals with minor infarction (n = 7. LVEDP = 7.7 ± 0.9 mmHg), forskolin (3 μ.mol/L) increased the maximal available INa+ to 109% ± 13% of baseline values. This increase was nearly the same in the group with significant infarctions (n = 7, LVEDP = 15.7 ± 1.6 mmHg) to 113% ± 6%. Thus, although we previously observed a reduction of the isoproterenol induced increase of INa+ in rats with significant myocardial infarctions, this increase remains the same when adenylyl cyclase is stimulated directly. This is consistent with a direct p-receptor down-regulation or desensitization. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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