Abstract

Norepinephrine (NE) is released from sympathetic nerves supplying arteries and veins. We studied temperature‐related (28–37 ºC) differences in NE release and clearance using amperometry to measure NE in vitro. Tissues from sham and DOCA‐salt hypertensive rats were studied. Peak NE currents in sham veins declined more with temperature compared to arteries. Peak currents in DOCA‐salt arteries also showed greater temperature sensitivity than those in sham arteries. Currents in sham veins and DOCA‐salt arteries increased faster, decayed more slowly and were more temperature sensitive than those in sham arteries. Idazoxan (blocks α2 adrenergic receptors, α2ARs) and cocaine (blocks the NE transporter, NET) accelerated current rise time in sham arteries only. NE current decay was accelerated by idazoxan in veins but not arteries at 37 ºC and in arteries but not veins at 28 ºC, with a smaller increase in DOCA‐salt arteries at 28 ºC than sham arteries. We conclude that control of NE release from peri‐arterial nerves is more complex and therefore more temperature‐sensitive than in peri‐venous nerves. DOCA‐salt hypertension impairs NE release and clearance in arteries but not veins. α2ARs functional as autoreceptors and possibly as a “clearance receptor” holding NE in the neuroeffector junction. Clearance of NE in sham arteries is NET‐dependent and in sham veins and DOCA‐salt arteries is α2 NE clearance receptor dependent.

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