Modelling volume‐loading hypertension with Guyton's model: role of whole body blood flow autoregulation

Abstract

Computer simulations offer a unique way to test the role of whole body blood flow autoregulation (WBFAR) in the pathogenesis of volume‐loading hypertension since it is not possible to block WBFAR experimentally. Using Guyton's large circulatory model, we analyzed, in the presence or absence of WBFAR, the hemodynamic and fluid volume changes in three classical models of volume‐loading hypertension. In the first model, hypertension was induced by reducing renal mass to 30% of normal and increasing salt intake by 6‐fold. In the presence of WBFAR, the development of hypertension (+30 mmHg) was characterized by an initial increase in cardiac output (CO) by ~30% followed by a secondary increase in vascular resistance (+25%). In the absence of WBFAR, there was a similar long‐term increase in blood pressure (BP). However, a nearly 2‐fold increase in CO and an increase in extracellular fluid volume by more than 30% were observed whereas vascular resistance decreased by 30% owing to the mechanical distension of blood vessels by the increased BP. Qualitatively similar results were obtained in two other models of volume‐loading hypertension: aldosterone infusion and Goldblatt 1 kidney ‐ 1 clip hypertension. From the simulations one may conclude that autoregulation limits the amount of fluid retention required to increase BP in order to achieve salt balance, but does not affect the final level of BP. (Supported by HL‐51971)