Key result
The density, coupling, and antiadrenergic effects of ventricular A1-adenosine receptors were not different in failing compared to nonfailing human myocardium.
Why the study?
Does the density and coupling of A1-adenosine receptors differ between nonfailing and failing human ventricular myocardium?
Does the density and coupling of A1-adenosine receptors differ between nonfailing and failing human ventricular myocardium?
Enhanced antiadrenergic effects of A1-adenosine receptors do not contribute to the reduction of cAMP-dependent positive inotropic effects in heart failure.
Findings do not support altered A1-adenosine receptor function in failing myocardium; hypothesis-generating for alternative cAMP pathway mechanisms in heart failure.
The purpose of the present study was to characterize adenosine receptors in human atrial and ventricular preparations as well as in nonfailing and failing human ventricular myocardium. Using the antagonist radioligand 3 H‐DPCPX, A 1 ‐adenosine receptors were identified in human atrial and ventricular myocardial membranes. The rank order of potency of agonists and antagonists as well as the influence of Gpp(NH)p on agonist high affinity binding were similar in atrial and ventricular myocardium, indicating that the same receptor type probably couples in a similar guanine nucleotide‐dependent way to different effectors producing the “direct” or “indirect” effects on myocardial force on contraction. The density and coupling of ventricular adenosine receptors as well as the antiadrenergic, “indirect” effect following their stimulation were not different in failing human myocardium, despite an increase in G iα ‐proteins. Thus, enhanced antiadrenergic effects of A 1 ‐adenosine receptors do not contribute to the reduction of cAMP‐dependent positive inotropic effects in heart failure.
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Böhm et al. (1993) studied Heart failure. Failing human ventricular myocardium vs. Nonfailing human ventricular myocardium was evaluated on Adenosine receptor density, coupling, and antiadrenergic effect. The density, coupling, and antiadrenergic effects of ventricular A1-adenosine receptors were not different in failing compared to nonfailing human myocardium.
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