We evaluated arteriolar myogenic responsiveness in normotensive, salt-loaded and hypertensive rats and investigated the potential influence of luminal blood flow or shear stress on myogenic responses under each of these conditions. Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Dietary salt did not affect mean arterial pressure (MAP) in WKY, whereas MAP in SHR was significantly higher and augmented by dietary salt. In all groups, box pressurization caused similar increases in MAP that were completely transmitted to the arterioles. After these pressure increases, large arteriole diameters decreased by 0-30% and intermediate arteriole diameters decreased by 21-27%. Arteriolar myogenic responsiveness was not different between WKY-LS and SHR-LS. Large arterioles in WKY-HS displayed an attenuated pressure-diameter relationship compared with that in WKY-LS. Large arterioles in SHR-HS displayed an augmented pressure-diameter relationship compared with that in SHR-LS. There were no correlations between resting flow or wall shear rate and the magnitude of initial myogenic constriction in any group or vessel type. The capacity for sustained myogenic constriction was unrelated to secondary decreases in flow (14-41%) or increases in wall shear rate (21-88%) in each group. We conclude that 1) dietary salt impairs the myogenic responsiveness of large arterioles in normotensive rats and augments the myogenic responsiveness of large arterioles in hypertensive rats, 2) hypertension does not alter arteriolar myogenic responsiveness in this vascular bed, and 3) flow- or shear-dependent mechanisms do not attenuate myogenic responses in the intact arteriolar network of normal, salt-loaded, or hypertensive rats.