Previous models for the transport across the arterial wall investigated the accumulation of macromolecule LDL (diameter > 22 nm) in the arterial structure through a leaky endothelial layer for the formation of atherosclerosis. The current study developed a transport model for smaller solutes (diameter of ∼ 7 nm or less) across an intact arteriole wall to elucidate how the structural components in the wall regulate the solute permeability of the arteriole wall. The structural components include endothelial surface glycocalyx and tight junctions between adjacent endothelial cells, the narrow layer of intima filled with the extracellular matrix (ECM), and the internal elastic lamina (IEL) with fenestral pores. The model incorporates the detailed arteriole wall structure and effective solute diffusion coefficients in different wall regions from the literature. The model predictions match well with the measured permeability of the porcine coronary arteriole to α-lactalbumin (diameter of ∼ 4 nm) and albumin (diameter of ∼ 7 nm). The predictions from the transport model for the arteriole wall also indicate that 1) the intima and IEL of the arteriole wall play a significant role in the modulation of arteriole wall permeability and 2) unlike in the capillary or post-capillary venule, whose wall is formed only by endothelial cells with some pericytes, endothelial surface glycocalyx is not the molecular sieve of the arteriole wall for macromolecules under physiological conditions. Furthermore, the simplified 1D model can be easily applied to predict the structural changes for the modified solute permeability in diseases.