Vascular flow reserve (VFR) is the relative increase in tissue perfusion from the resting state to a state with maximum vasodilatation. Longstanding hypertension reduces the VFR, which in turn reduces the maximum working capacity of the tissue. In principle, both inward arteriolar remodelling and rarefaction of the microvascular network may contribute to this reduction. These processes are known to occur simultaneously in the microcirculation of the hypertensive individual and both cause a reduction in the luminal trans-sectional area available for perfusion. Which of them is the main factor responsible for the reduction in VFR is, however, not known. Here we present simulations performed on large microvascular networks to assess the VFR in various situations. Particular attention is paid to the VFR in networks in which the vessels have structurally adapted to a sustained increase in pressure by inward eutrophic remodelling (IER), i.e. by redistributing the same amount of wall material around a smaller lumen. Collectively, the results indicate that the IER may not per se be the main factor responsible for the hypertensive reduction in VFR. Rather, it may be explained by the presence of arteriolar and capillary rarefaction.

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Arterioles are normally thought of as having a constant structural diameter between branch points. In unbranched rat cremaster arterioles, however, structural diameter increases downstream along the vessel (upstream tapering) without change in cross‐sectional area of the vascular wall (1). We addressed the possible functional consequence of this configuration by flow‐simulations comparing myogenically active vessels of uniform structural radius with those having an upstream tapering shape. In our model cross‐sectional area of the vascular wall remains invariant along the vessel and the flow is the same in all cases.ResultsThe vascular wall material can be arranged in an upstream tapering configuration such that circumferential wall stress is uniform along the vessel. The stress remains uniform during flow‐autoregulation when perfusion pressure is changed. In contrast, when the structural radius is uniform along the vessel wall stress is much higher upstream than downstream, and this difference is maintained under variations in perfusion pressure.ConclusionIn a myogenically active vessel upstream tapering of the inner radius allows the circumferential wall stress, and hence possibly the contractile state of the wall smooth muscle cells, to remain constant along the vessel at a given pressure. This is not the case for a vessel with a uniform radius. The upstream tapering shape is consistent with the vascular wall cells having a uniform point of operation as regards stress‐induced myogenic contraction.