title: Dominant role of the kidneys and accessory role of whole-body autoregulation in the pathogenesis of hypertension.
abstract: In this paper I have presented two closely related themes both of which seem to be fundamental in understanding the pathophysiology of hypertension. The first theme is the dominant role of the volume-excretion function of the kidneys in setting the long-term arterial pressure level. That is, each person in general has a rather steady intake of salt, water, and those other constituents that make up extracellular fluid. When the arterial pressure is normal, the kidney excretion of these constituents is exactly the correct amount to balance the intake of each of them. When the pressure is too great, there is more loss than gain, and the body fluid volume decreases; therefore, the pressure falls until the exact balance point is reached again; it is only at this balance point that the loss and gain are equal. At any pressure below the balance point, volume gain is greater than loss, and the pressure will continue to rise until the exact balance level is again reached. This capability of the kidney mechanism to return the pressure all-the-way back to the level of balance between input and output--not merely part-way back--is called the "infinite gain" characteristic of this pressure control system, and the level to which the pressure is controlled is called the "set-point" of the system. In pathophysiological states, the set-point for pressure control can be increased to hypertensive levels as a result of (1) a pathophysiological change in renal function or (2) increased salt and volume intake; then hypertension will ensue. Other abnormalities of circulatory function that do not affect one of these two factors cannot cause chronic hypertension because of the infinite gain feature of the renal-volume mechanism for pressure control. One such condition that does not cause hypertension without some concurrent abnormality that affects renal function is a primary increase in total peripheral resistance. The second theme is that whole-body autoregulation causes the blood flow in all parts of the body to return or remain near to normal when high arterial pressure tries to increase the flow. It does this by increasing the resistance in all parts of the peripheral arterial tree. Therefore, in effect, autoregulation converts any tendency to high cardiac output hypertension into high resistance hypertension. Yet, in so far as is now known, the pressure level will be the same with or without autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
authors.affiliation: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
authors.forename: A C
authors.initials: AC
authors.lastname: Guyton
mesh_terms: D002908:Chronic Disease; D005110:Extracellular Space / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D012084:Renin-Angiotensin System; D012982:Sodium, Dietary / Q000008:administration & dosage; D014655:Vascular Resistance
chemical_list: D012982:Sodium, Dietary