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Background While b-adrenergic blockade is a cornerstone of heart failure therapy, its therapeutic role in chronic mitral regurgitation remains questionable. Animal studies and a small clinical trial have demonstrated cardiac functional improvement with b1-adrenoceptor blocker metoprolol in chronic mitral regurgitation [1,2]. How b1AR-blockade halts functional decline of the volume-overloaded, eccentric hypertrophied heart is not well understood; anti-oxidant effects of b-blockade (bB) may play a role. We recently demonstrated that volume-overload cardiac stress induces re-localization and microdomain-specific oxidation of the nitric oxide receptor soluble guanylyl cyclase (sGC) in the failing heart [3,4]. Given that nitric oxide-cyclic guanosine monophosphate (NO-cGMP) modulates cardiac contractility and protects against cardiac hypertrophy, we hypothesized that b1AR-blockade prevents oxidation of sGC and promotes myocardial NO-cGMP signaling in a microdomain-specific fashion.

Chronic beta-adrenergic blockade prevents volume overload-induced re-localization and oxidation of soluble guanylyl cyclase