Toward a broader understanding of aldosterone in congestive heart failure

Abstract

Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na + in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na + appetite, Na + and H 2 O excretion and sympathetic nerve activity, and the regulation of TNF-α production from central and/or peripheral sources. Extra-adrenal steroidogenesis and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDO's contribution to the pathophysiology of congestive heart failure will undoubtedly emerge.

Spironolactone diminishes spontaneous ventricular premature beats by reducing HCN4 protein expression in rats with myocardial infarction

“…a subsequent study showed that the combination of VPB plus couplets is an independent indicator of the total mortality rate after acute Mi (27). However, the mechanisms of this effect are unclear; several mechanisms may account for the reduction in mortality caused by spironolactone, such as attenuated sym pathetic tone (28,29) and improved parasympathetic activity (30,31), or direct inhibition of the Mi-induced increase in T-type calcium current (32,33). in this study, we found a correlation between improvements in the survival rate ( Fig.…”

Paraventricular nucleus, stress response, and cardiovascular disease

“…The effects of AT 1 receptor activation may involve local production of superoxide [45]. Aldosterone, acting via mineralocorticoid receptors in the PVN, may also increase sympathetic activity [78]. Thus, the PVN has a pivotal role in the feedforward relationship between the renin-angiotensin-aldosterone axis and the sympathetic output controlling renin release, blood flow, and tubular Na + reabsorption by the kidney [35].…”

Effect of furosemide and high-dosage pimobendan administration on the renin-angiotensin-aldosterone system in dogs

“…The role of the RAAS as a cause of fluid retention, endothelial and baroreceptor dysfunction, and vascular and myocardial remodeling in patients with chronic heart failure is well accepted. [1][2][3][4][5][6] The RAAS can also be activated pharmacologically by drugs often used to treat heart failure. These drugs include vasodilators such as amlodipine 7 and hydralazine 8 and diuretics such as furosemide.…”