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Regulation of norepinephrine levels in synaptic clefts of dog vascular tissue

1982; American Physical Society; Volume: 242; Issue: 2 Linguagem: Inglês

10.1152/ajpheart.1982.242.2.h233

1522-1539

Duane K. Rorie, Gertrude M. Tyce,

Cardiac Ischemia and Reperfusion

The overflow of endogenous norepinephrine (NE) from superfused dog pulmonary artery and saphenous vein in response to electrical stimulation and the content of NE remaining in the tissue after stimulation were measured using liquid chromatography with electrochemical detection. Overflow of NE was 0.15-0.22 and 0.14 to 0.30 ng/min in pulmonary artery and saphenous vein, respectively, during stimulation. Release of NE (measured in the presence of cocaine and corticosterone to block removal of NE from the synaptic cleft) was greater in the pulmonary artery (0.50-0.87 ng/min) than in saphenous vein (0.39-0.51 ng/min). NE overflow decreased after the first 4 min of continuous stimulation in saphenous vein but not in pulmonary artery. As only 2.26% of the NE content of vein overflowed during stimulation, depletion of NE or deterioration of the preparation seemed unlikely. Presynaptic alpha- or beta-receptor blockade did not change the pattern of NE overflow. Thus in the saphenous vein, but not in the pulmonary artery, removal of NE from the synaptic cleft appears to be facilitated during electric stimulation. This suggests the existence of a new mechanism, possibly related to enhanced catechol methyltransferase activity, which regulates NE levels in the synaptic cleft in saphenous vein but not in pulmonary artery.