Large diameter elastic arteries can produce strong contractions indefinitely at a high energy economy by formation of latchbridges. Whether downstream blood vessels also use latchbridges remains unknown. The zero pressure medial thickness and lumen diameter of rabbit saphenous artery (SA), a muscular branch of the elastic femoral artery (FA), were, respectively, ~2-fold and 1/2-fold that of the FA. In isolated FA and SA rings, KCl rapidly (<16 sec) caused strong increases in isometric stress (1.2 x 10⁵ N/m²) and [Ca²⁺]_i (250 nM). By 10 min, [Ca²⁺]_i declined to ~175 nM in both tissues, but stress was sustained in FA (1.3 x 10⁵ N/m²) and reduced by 40% in SA (0.8 x 105 10⁵ N/m²). Reduced tonic stress correlated with reduced myosin light chain (MLC) phosphorylation in SA (28% vs. 42% in FA), and simulations using the 4-state kinetic latchbridge model supported the hypothesis that latchbridge formation in FA, but not SA, permitted maintenance of high stress values at steady-state. SA expressed more MLC phosphatase than FA, and permeabilized SA relaxed more rapidly than FA, suggesting that MLC phosphatase activity was greater in SA than FA. The ratio of fast-to-slow myosin isoforms was greater for SA than FA, and upon quick-release, SA redeveloped isometric force faster than FA. These data support the hypothesis that maintained isometric force was 40% less in SA than FA because expressed motor proteins in SA do not support latchbridge formation.