Quantitative approaches for studying the microcirculation include computational methods and integrative experimental models. This presentation will provide examples of applying both approaches to better understanding the causes and effects of microvascular network pattern formation. The first objective will be to highlight the use of a computational method for gaining new insight into the relationship between network patterns and resistance in hypertension. Microvascular rarefaction, defined by a loss of vessels, is a common characteristic of hypertension and has been linked to elevated microvascular resistance. However, vessel loss in mesenteric microvascular networks from adult spontaneously hypertensive rats (SHRs) versus age-matched normotensive Wistar-Kyoto (WKY) controls is accompanied by an increase in low resistance arterial-venule shunts. Using a computational model that can account for intact network patterns, the total resistances were compared in SHR versus WKY networks. For simulations with uniform vessel diameter and with the diameters based on reported intra-vital measurements, SHR resistance was not increased compared to the WKY level. This result challenges the paradigm that microvascular networks experience increased resistance during hypertension. Still, a question remains – What causes the vessel loss and pattern alterations in the SHR? An answer might be vascular pericytes. SHR networks also display altered pericyte expression of neuron-glia antigen 2 (NG2) implicating them as a critical cell type. The second objective of the presentation will be to introduce the rat mesentery culture model as a novel experimental tool for determining the effect of NG2 inhibition on microvascular network growth. After 3 days in culture with minimum essential media, Wistar mesenteric microvascular networks remain viable and intact. More importantly, growth factor induced endothelial cell sprouting can be inhibited by antibody blocking of NG2 on pericytes. This result confirms the importance of NG2 as a functional regulator of capillary sprouting and establishes the rat mesentery culture model as a novel tool for mechanistic studies investigating pericyte-endothelial cell interactions at specific locations within a microvascular network. Overall, the use of computational modelling and the rat mesentery culture model in these studies emphasizes the value of integrating a quantitative and systems level perspective in microvascular research.