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Cell Physiol Biochem. 2012;29(5-6):833-40. doi: 10.1159/000178483. Epub 2012 May 11.

Spironolactone prevents aldosterone induced increased duration of atrial fibrillation in rat.

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1
Department of Internal Medicine III, University of Cologne, Cologne, Germany.

Abstract

BACKGROUND:

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The Renin-Angiotensin-Aldosterone-System plays a major role for the atrial structural and electrical remodelling. Recently elevated aldosterone levels have been suggested to increase the risk for the development of AF.

METHODS:

Rats were treated with aldosterone by means of an osmotic minipump (0.5μg/h) over a period of 4 weeks. AF was induced by transesophageal burst pacing. Action potentials (AP) were recorded from left atrial preparations with microelectrodes. Atrial collagen was quantified by histological studies.

RESULTS:

Aldosterone treatment resulted in hypertrophy as indicated by an increased ratio of heart weight/tibia length and doubled the time until the AF converted spontaneously into sinus rhythm (85.8±13.4 s vs. 38.3±6.9 s, p<0.01). This was associated with a significant shortening of the AP (APD90 26.2±1.1 vs. 31.2±1.9, p<0.05) and an increased protein expression of Kir2.1 and Kv1.5. Atrial collagen deposition was significantly greater in aldosterone-treated rats. The alterations could be prevented by additional application spironolactone.

CONCLUSIONS:

The results of the present study suggest that in addition to the structural remodelling aldosterone also promotes AF by altering repolarising potassium currents leading to action potential shortening.

PMID:
22613983
DOI:
10.1159/000178483
[Indexed for MEDLINE]
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