Calcium channel blockers (CCBs) reduce afterload but not preload in vivo, suggesting that arteries and veins use different mechanisms to mediate contraction. We investigated this hypothesis using pressurized small mesenteric arteries (MA) and veins (MV) from male Sprague Dawley rats. Both MA and MV contracted robustly to 60 mmol/L KCl. Nifedipine (1 nmol/L – 1 μmol/L) and diltiazem (10 nmol/L – 10 μmol/L) each maximally reversed the KCl‐induced contraction in MA by 93%. Although we detected an abundance of L‐type Ca2+ channel mRNA and protein by RT‐PCR and Western blot, respectively, MV did not dilate significantly to either CCB. Whole‐cell patch‐clamp studies revealed that Ca2+ current (ICa) density in freshly dissociated smooth muscle cells from MV was 68% less than in cells from MA (MV, −3.8±0.7 pA/pF; MA, −11.7±3.0 pA/pF). However, the ICa was similarly sensitive to block by 100 nmol/L nifedipine (percent block: MA, 50%; MV, 60%). The KCl‐induced contraction in MA was prevented by removal of extracellular Ca2+, whereas 60±7% of the response persisted in MV. This persistent contraction was eliminated by EGTA (0.5 mmol/L) or thapsigargin (1 μmol/L). Thus, MV express functional L‐type Ca2+ channels, but these channels do not contribute to KCl‐induced contraction. Instead, a unique mechanism linking membrane depolarization to intracellular Ca2+ release may exist in veins.