Endocrine Abstracts

Introduction: Aldosterone (Aldo) decreases the rate of repolarization in rabbit cardiomyocytes and significantly increases the duration of the monophasic action potential in patients with supraventricular arrhythmias, few minutes after its intravenous administration, implying for a non-genomic action. We have previously found a positive linear regression between left ventricular systole duration and plasma Aldo levels in NZW rabbits. To investigate the veracity of the above finding on cardiac cycle (CC) phases and elucidate the underlying mechanism we employ the HL-1 cell line of mouse atrial cardiomyocytes.

Materials and methods: Confluent beating HL-1 cells were stained with 68 μM di-8-ANEPS in 68 μM Pluronic F-127. Cell beating and the accompanied fluorescent intensity changes, were recorded with a specialized high frequency sampling (1 kHz) CMOS camera (NeuroCMOS-SM128f, Redshirt Imaging, Inc., USA) coupled to a fluorescent microscope (AxioExaminer Z1, Carl Zeiss Microimaging GmbH, Germany). 15 optical recordings, of 2 s duration, were taken 1 min apart. 50 μM Aldo in Claycomb’s medium was added between the third and fourth recording (control received only the same volume of medium). CC total duration, contraction period (corresponding to cardiac systole) as well as relaxation period and duration of the ‘quite’ state of the cells (both corresponding to cardiac diastole) were calculated.

Results: Our results show that Aldo increases the total duration of the CC (P<0.001 (Z-score (standard score) and Spearman’s ρ)) almost immediately after its addition to the cells lasting up to 14 min, when recordings were stopped. This increase is attributed to the ‘quite’ state of the cells corresponding to the diastolic phase of the CC.

Conclusion: Aldo causes a reduction of the beating frequency of the HL-1 cells. Their prompt response to Aldo denotes a non-genomic action. Taking into account of our previous finding, this action can be attributed to elongation of the first part of cardiac diastole (protodiastole).

Disclosure: This work was supported by the Aristotle University of Thessaloniki Research Committee (grant number 89791).