We have studied the mechanism of release of plasminogen activator (PA) activity induced by epinephrine in the perfused rat hindleg model. Epinephrine perfusion at the dose of 12.5 μM caused a slighter effect on PA activity but an immediate increase in the perfusion pressure. At 25 μM, epinephrine induced a marked increase in PA activity that reached the maximum level at the end of the drug perfusion. The same response was induced by repeated stimulations with epinephrine (25 μM) only if the second stimulus was given 20-25 min apart from the first one. PA release could be blocked by propranolol (300 μM), a nonspecific β-blocker, and not by phentolamine, a nonspecific α-blocker, unless used at very high concentrations (1,250 μM). Perfusion with dibutyryl adenosine 3',5'-cyclic monophosphate (DbcAMP) alone induces an immediate and transient increase in PA activity, but no potentiation could be demonstrated if theophylline was perfused together with epinephrine. The released PA has been characterized on the basis of molecular weight and immunological criteria as t-PA- and u-PA-like molecules in basal conditions. Epinephrine perfusion induced an increase only in the t-PA-like protein. These data indicate that the release of t-PA-like activity observed after epinephrine perfusion is mainly mediated by β-receptors and is independent from its vasoactive action.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Publication status||Published - 1989|
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