Question: 

There is increasing evidence that aldosterone might be an important player in the development of cardiomyopathies. Particularly, chronically elevated levels of aldosterone (hyperaldosteronism) contribute to the generation of atrial fibrillation, tachycardia, hypertrophy or fibrosis. In this study we explored the impact of hyperaldosteronism on isolated cardiac myocytes.

Methodology: 

We elevated blood plasma levels of adult rats by implanting osmotic mini-pumps in 8 week old rats for 8 weeks (1,5 mg/h aldosterone). For the investigation of cellular alterations we isolated ventricular and left plus right atrial myocytes to study their cellular calcium handling, contractility and electrical properties.

Result: 

In ventricular myocytes we observed a significant drop of resting calcium, 1st amplitude and steady-state amplitude of global electrically induced calcium transients. For atrial myocytes of the right atrium such changes were more pronounced while surprisingly, the left atrial myocytes displayed even less effects than ventricular cells. Concomitantly, the contractility of right atrial myocytes was also impaired. Here, the contraction-frequency relationship (0.2 - 2 Hz) was negative and their diastolic sarcomer length was severely increased. In patch-clamp experiments, atrial myocytes showed substantial changes in their action potentials (AP). Interestingly, the early phases of repolarisation were largely shortened (~50% change) in left and right atrial cells. In addition, right atrial cells showed a reduced action potential rise time and cell membrane capacitance was significantly reduced (~30%).

Conclusion: 

We demonstrated for the first time the differential impact of hyperaldosteronism on ventricular, right and left atrial cardiac myocytes.