Abstract

Cardiac adenosine is formed both by an oxygen-sensitive (AMP----adenosine) and by an oxygen-insensitive (S-adenosylhomocysteine----adenosine) pathway. The phasic adenosine release during beta-adrenergic stimulation with isoproterenol is closely linked to coronary venous PO2 (isolated heart) and can be almost fully prevented when diastolic aortic pressure is maintained constant (heart in situ). During pressure autoregulation the transmural gradient of free adenosine is only increased when the autoregulatory reserve is exhausted. The critical PO2 below which adenosine formation is enhanced was found to be 3 mm Hg (isolated cardiomyocytes). Collectively, these data indicate that the formation of adenosine is not primarily coupled to the energy expenditure of the heart but to the supply/demand ratio for oxygen.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call