Dose torasemide have an aldosterone receptor antagonist ?

Abstract

Background: We reported that mineralocorticoid receptor antagonist spironolactone inhibits the transcardiac extraction of aldosterone (ALD) in patients with congestive heart failure (CHF). In the TORIC study, torasemide had more beneficial effect on mortality and morbidity of CHF patients than furosemide. However, the mechanism of the beneficial effect of torasemide remains unknown. Method: To evaluate whether the torasemide has an ALD receptor antagonist, we studied 50 CHF patients who had been randomly administered furosemide (n = 25) or torasemide (n = 25). Results: There was no difference of patients characteristics, other treatments, left ventricular ejection fraction, and plasma levels of BNP in the aortic root (AO) between the two groups. In the furosemide group, plasma ALD was significantly lower in the coronary sinus (CS) than in the AO (96 ± 11 vs. 75 ± 12 pg/mL, p < 0.001), suggesting that ALD is extracted through the heart. In contrast, there was no difference of plasma ALD between the AO and CS in the torasemide group (83 ± 11 vs. 78 ± 12 pg/mL, p = 0.17), suggesting that the extraction of ALD through the heart is inhibited by torasemide. In addition, there was a significant negative correlation between dose of torasemide and the transcardiac gradient (Ao-CS) of ALD in the torasemide group (r = -0.56, p < 0.01). Conclusion: These findings suggest that torasemide has an ALD receptor antagonist in the failing heart in patients with CHF.