Endothelin-1 and Norepinephrine Overflow from Cardiac Sympathetic Nerve Endings in Myocardial Ischemia
Figure 1
Summarizing scheme illustrating the interaction between the ET-1 system and carrier-mediated NE release in protracted myocardial ischemia. Stimulation of ETARs existing in sympathetic nerve endings by endogenously generated or exogenously applied ET-1 increases neuronal NHE activity, thus potentiating carrier-mediated NE release. In contrast, exogenously applied big ET-1 is converted to ET-1 by cell surface ECE-1, and this ET-1 preferentially binds to ETBRs located on NOS containing cells to produce NO. Endogenously generated NO works to prevent carrier-mediated NE release. NCX, Na+/Ca2+ exchanger; VMAT: vesicular monoamine transporter.
