Arterial pressure regulation: Overriding dominance of the kidneys in long-term regulation and in hypertension

https://doi.org/10.1016/0002-9343(72)90050-2Get rights and content

Abstract

The body is endowed with many different arterial pressure regulating mechanisms, some of which operate rapidly, some slowly; some of which operate at low pressure ranges, some at normal pressure ranges, and some at high pressure ranges; some of which have weak feedback gains, some of which have moderate feedback gains, and one of which has infinite gain when sufficient time is allowed for its control functions to reach the state of equilibrium. The infinite gain pressure control system is based on the effect of arterial pressure on renal output of water and salt. If the arterial pressure becomes too high, the output becomes greater than the net intake of water and salt, and the body becomes progressively dehydrated until this dehydration causes the pressure to return all the way to normal. It is this “all the way” response that is the cause of the infinite gain. Because of the infinite gain of this control mechanism, it is the one that determines the long range level of arterial pressure.

Many factors can affect the operation of the renal-body fluid mechanism for arterial pressure regulation. These include nervous effects acting on the kidney, hormonal factors acting on the kidneys, pathology of the kidney, and so forth. However, the principle of infinite gain in this system requires that, in some way, all long-term arterial pressure regulation must involve the balance between intake and output of water and salt and almost invariably involves the kidneys.

References (11)

  • C Heymans et al.

    Reflexogenic Areas of the Cardiovascular System

    (1959)
  • K Segawa et al.

    Dynamic performance and stability of cerebral ischemic pressor response

    Amer J Physiol

    (1961)
  • AW Cowley et al.

    Open-loop analysis of the renin-angiotensin system in the dog

    Circ Res

    (1971)
  • TG Coleman et al.
  • JH Laragh et al.

    Hypotensive agents and pressor substances: the effect of epinephrine, norepinephrine, angiotensin II, and others on the secretory rate of aldosterone in man

    JAMA

    (1960)
There are more references available in the full text version of this article.

Cited by (0)

This study was supported by grants-in-aid from the U.S. Public Health Service and the American Heart Association.

1

From the Department of Physiology and Biophysics, University of Mississippi School of Medicine, Jackson, Mississippi.

View full text