Hypertension: A Disease of Abnormal Circulatory Control

Abstract

There is a widespread belief that some of the rapidly acting pressure control mechanisms such as the baroreceptor feedback mechanism and the reninangiotensin mechanism are also the primary determinant factors for longterm arterial pressure control. But recent theoretical analyses, supported by great amounts of experimental and clinical evidence, have shown that the primary controller of the longterm pressure level is a renal-body fluid volume feedback mechanism for pressure control. This mechanism operates simply as follows: an increase in arterial pressure causes the kidneys to excrete markedly increased quantities of urine. This, in turn, decreases the level of body fluids and eventually decreases the arterial pressure toward normal. However, the short-term arterial pressure control mechanisms obscure this mechanism in acute experiments. Therefore, acute experiments have, until recently, failed to demonstrate the extreme importance and potency of the fluid mechanism. The renal-body fluid volume mechanism for pressure control is a feedback control system of the integral control type that, under appropriate conditions, has infinite capability to return the arterial pressure to its reference pressure level. This reference pressure level is determined by two primary factors: (1) the urinary volume load; and (2) the renal function curve that relates arterial pressure to the urinary volume load. The second of these is usually by far the more important. Therefore, the kidneys play an almost insuperable role in longterm arterial pressure regulation and in hypertension. Nonrenal hypertensive abnormalities can be shown both theoretically and experimentally to cause hypertension by altering either kidney function or fluid intake. Studies indicate that the portions of the kidney most responsible for arterial pressure control are the pretubular segments: the afferent arterioles and the glomerular membrane. Therefore, one can predict that most types of hypertension mechanisms must in one way or another result from primary or secondary abnormal function of one of the pretubular elements of the kidney.