Computer models for designing hypertension experiments and studying concepts.
This paper demonstrates how computer models along with animal experiments have been used to work out the conceptual bases of hypertensive mechanisms, especially the following: (1) The renal-fluid volume pressure control mechanism has a feed-back gain for pressure control of infinity. Therefore, the chronic level to which the arterial pressure is controlled can be changed only by altering this pressure control mechanism. (2) An increase in total peripheral resistance is not sufficient by itself to cause hypertension. The only resistances in the circulatory system that, when increased, will cause hypertension are those along a restricted axis from the root of the aorta to Bowman's capsule in the kidneys. (3) Autoregulation in the peripheral vascular beds does not increase the arterial pressure in hypertension. However, autoregulation can convert high cardiac output hypertension into high peripheral resistance hypertension. (4) In a computer simulation that cannot yet be performed in animals, a simulated hypertension caused by a combination of increased renal afferent and efferent arteriolar resistances has characteristics that match almost exactly those of essential hypertension.
Guyton
A C
AC
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216.
Montani
J P
JP
Hall
J E
JE
Manning
R D
RD
D000818:Animals; D001160:Arterioles / Q000473:pathology; D001794:Blood Pressure; D002302:Cardiac Output; D003198:Computer Simulation; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D006984:Hypertrophy; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology; D008954:Models, Biological; D014655:Vascular Resistance; D014882:Water-Electrolyte Balance