We studied sympathetic transmission to mesenteric arteries (MA) and veins (MV) from sham and DOCA-salt rats. Amperometric methods and video imaging were used to monitor norepinephrine (NE) release and neurogenic constriction which were elicited by focal electrical stimulation (FES, 60 pulses at 0.5–20 Hz) in vitro. MV were more sensitive than MA to FES-evoked NE release and neurogenic constriction. There were no differences in responses between sham and DOCA-salt MV. More NE was detected in DOCA-salt vs. sham MA but there were not differences in constrictions. The latency for constriction onset was longer for MV than MA but constriction rate was faster in MV. NE transporter (NET) inhibition and/or treatment with α2 adrenoceptor antagonists produced greater increases in detectable NE in MA vs. MV; α2 adrenoceptor antagonist effects were impaired in MA and MV from DOCA-salt rats. Tyrosine hydroxylase staining revealed a denser plexus of sympathetic nerves in MA than MV. The plexus in MV had a circumferential arrangement. The plexus in MA did not have a preferred arrangement. The data indicate that increased sensitivity of MV vs. MA to nerve stimulation is due to increased NE availability in MV. NET and α2-autoreceptors play a greater role in regulating NE junctional levels in MA than MV. Increased NE availability in MA would contribute to increased peripheral resistance in DOCA-salt hypertension. Differences in kinetics and arrangement of perivascular nerves may also contribute to differential sympathetic control of MA and MV.