Ungerer M, Richardt G
Medizinische Klinik II, Medizinische Universität zu Lübeck.
Z Kardiol. 1996;85 Suppl 6:171-5.
Adenosine exerts most of its cardiac effects via direct interaction with sympathetic neurotransmission: Release of norepinephrine is inhibited in presynaptic neurons, and catecholamine-induced activation of adenylyl cyclase is inhibited in postsynaptic effector cells. While presynaptic effects fade rapidly during ischemia, postsynaptic antagonism to catecholamines remains an important protective element during sustained ischemia.