Spironolactone works through a mechanism different than the adrenergics.
You said of the ABC approach, "This includes also diuretics." That's why Spironolactone was included.
Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule. Aldosterone interacts with a cytoplasmic mineralocorticoid receptor to enhance the expression of the Na+, K+-ATPase and the Na+ channel involved in a Na+ K+ transport in the distal tubule . Spironolactone bind to this mineralcorticoid receptor, blocking the actions of aldosterone on gene expression. Aldosterone is a hormone; its primary function is to retain sodium and excrete potassium in the kidneys.
The lack of a decrease in the neuroendocrine prognostic markers, norepinephrine and endothelin-1, suggests that the beneficial effects of spironolactone are mainly related to mechanisms independent of the adrenergic and endothelin systems. The escape of AII and aldosterone, probably reflecting activated feedback mechanisms, confirms the specific activity of spironolactone on the renin-angiotensin-aldosterone system and supports the hypothesis that the beneficial effects of spironolactone on the progression of heart failure are mediated by the blockade of aldosterone receptors.
Beneficial neurohormonal profile of spironolactone in severe congestive heart failure: Results from the RALES neurohormonal substudy