The effect of arterial hypertension on the splanchnic circulation is assessed. In human essential hypertension, splanchnic vascular resistance rises in proportion to the blood pressure, and the transvascular escape rate of plasma proteins is increased. The various animal models of hypertension show variable results, but in general support the concept that vascular resistance changes in the splanchnic organs are similar in direction and magnitude to pressure changes. This is especially true in longer-term chronic experiments. These resistance changes appear to result from increased responsiveness of the arterioles to a variety of constrictor influences, and they may result from either structural or functional changes. Hypertension appears to alter splanchnic arteriolar permeability via a pressure-dependent mechanism. These vessels may also undergo degenerative histological changes. Capillaries and small venules experience increased endothelial permeability via a pressure-independent mechanism that is not mediated by angiotensin II. In addition to the resistive and exchange alterations, the capacitance function of splanchnic veins is reduced, probably via a structural change. Much work remains to be done before the characterization is complete. Especially needed are studies of individual organs with respect to vascular resistance, exchange, and capacitance alterations in the various models of hypertension.