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. 2006 Sep 4;203(9):2191–2200. doi: 10.1084/jem.20060077

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Copyright © 2006, The Rockefeller University Press

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Figure 3. — Mechanisms of rt-PA–induced NE release in guinea pig heart synaptosomes. (A) Concentration response curves for the NE-releasing effect of rt-PA and plasmin (each at 0.1–10 μg/ml) in guinea pig (GP) heart synaptosomes. As opposed to rt-PA, plasmin did not elicit NE release. Points are means (± SE [error bars]; n = 10 for r-tPA and n = 4 for plasmin). (B) Effects of various inhibitors on the NE-releasing effect of 10 μg/ml r-tPA. Preincubation with the inhibitors reduced the rt-PA–induced NE release from guinea pig heart synaptosomes. 100 nM Ω-conotoxin (ω-CTX), 10 μM BAPTA-AM, 300 nM desipramine (DMI), 30 μM 5-(N-ethyl-N-isopropyl)-amiloride (EIPA), and 1 μM cariporide (HOE642) each significantly inhibited rt-PA–induced NE release. In contrast, 0.2 μM α₂-antiplasmin (α₂-AP) did not affect the NE-releasing effect of rt-PA. Bars are means (± SE; n = 3–12) of percent increases in NE release above basal level. *, P < 0.05 versus rt-PA alone.