title: Structural adaptation of vascular networks: role of the pressure response.
abstract: Structural reductions in vessel luminal diameters in response to elevated pressure may play a role in the elevation of peripheral resistance generally observed in hypertension. In the present study, a theoretical model is used to simulate the effect of increased driving pressure on flow resistance in microvascular networks. The angioarchitecture (lengths and diameters of all segments, topology) of microvascular networks (n=6) in the rat mesentery was recorded by intravital microscopy. The model simulation of vascular adaptation in response to local wall shear stress, transmural pressure, and tissue PO(2) was used to predict changes in network pressure drop and flow resistance for a given change of driving pressure (DeltaP). For DeltaP increasing from 15% to 190% of the normotensive value, a 3.3-fold increase in flow resistance was observed (structural autoregulation). If vascular reactivity to pressure was suppressed, the resistance increase was abolished. Suppressing pressure sensitivity also led to a rise in mean capillary pressure at normal driving pressure from 23.8+/-7.3 mm Hg to 34+/-6.9 mm Hg. These results indicate that low capillary pressure levels as well as structural autoregulation depend on vascular responses to circumferential wall stress (corresponding to pressure). This tendency of peripheral vascular beds to increase flow resistance for a given increase of bulk flow or driving pressure may amplify and stabilize blood pressure elevation in the development of hypertension.
authors.affiliation: Department of Physiology, Freie Universität Berlin, Berlin, Germany. pries@zedat.fu-berlin.de
authors.forename: A R
authors.initials: AR
authors.lastname: Pries
authors.forename: B
authors.initials: B
authors.lastname: Reglin
authors.forename: T W
authors.initials: TW
authors.lastname: Secomb
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D008955:Models, Cardiovascular; D051381:Rats; D017208:Rats, Wistar; D013152:Splanchnic Circulation / Q000502:physiology*; D013314:Stress, Mechanical; D014655:Vascular Resistance / Q000502:physiology