Reports from several laboratories indicate that the early part of smooth muscle contraction is achieved by normally cycling crossbridges, while the later part is subserved by slowly cycling or latch-bridges. We have recently found that the early bridges are responsible for almost 75% of the maximum shortening of the muscle. The latch bridges appear to be responsible for force production. The earliest change in the mechanical properties of caudal arteries from spontaneously hypertensive rats (SHR) is an increase in maximum shortening ability (delta Lmax), at a time when there is no detectable change in maximal isometric tetanic tension (Po). This substantiates the hypothesis that changes in Po are late indices of disease. The increased delta Lmax is associated with increased maximal velocity of shortening (Vo) of early cross-bridges, whereas latch bridge activity is normal. This provides the first subcellular explanation for the increase in delta Lmax. Since hypertension must result from narrowing of blood vessels, delta Lmax is, parenthetically, the important variable to study. Changes in Po, while contributing to increased vascular wall stiffness, do not directly account for the increased resistance. The cause of the increased cycling rate of crossbridges is probably increased myosin ATPase activity, or myosin light-chain phosphorylation by the specific kinase. Studies in helical sections of caudal, and segments of mesenteric resistance arteries provided similar results, confirming the suitability of caudal arteries as a model of resistance vascular units. The larger vessel is of course much easier to work with.