AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 4 643-R662, Copyright © 1986 by American Physiological Society
Interrelationship of blood flow, juxtaglomerular cells, and hypertension: role of physical equilibrium and Ca
J. C. Fray, D. J. Lush and C. S. Park
Recent experimental evidence has provided important clues as to the role of
electrolytes, particularly Ca, in the regulation of blood flow, renin
secretion, and blood pressure. The smooth muscle cells of arterioles in
general and the juxtaglomerular cells in the renal afferent arterioles have
been shown to have Ca channels sensitive to voltage, hormones, and stretch.
This paper reviews a model that utilizes these features along with a
fundamental law of physics to point to some plausible explanations for some
interesting experimental observations on renal blood flow, renin secretion,
and hypertension. The chief features of the model are that in the steady
state the arteriole must achieve a stable physical equilibrium in which the
forces tending to distend the vessel (transmural pressure) counterbalance
the forces tending to prevent distension (wall tension); the wall tension
consists of a passive and an active component, the latter of which is
sensitive to stretch of the vessel; and stretch activates the opening of
stretch-sensitive Ca permeability channels that promote the influx of Ca to
trigger active tension development. Thus Ca is the signal that couples
stretch to contraction. This latter feature is the so-called myogenic
response. Altered equilibrium may be initiated either by a rise in
perfusion or tissue pressure to alter the distending force or by a rise in
cytosolic Ca to increase active tension development and the constricting
force. Several factors may initiate disequilibrium, some of which are
discussed. Equilibrium is soon reestablished, however, at a new steady
state. The model predicts curves for renal blood flow autoregulation and
renin secretion in response to changes in renal perfusion pressure, tissue
pressure, extracellular Ca, and blockers and promoters of Ca influx and Ca
efflux. These predictions agree well with existing experimental evidence
and suggest new experiments. The model provides a theoretical basis for
explaining the steady-state blood pressure profile observed in renovascular
hypertension and perhaps in other forms of hypertension as well. The model
also provides a theoretical basis for understanding the
volume-vasoconstriction approach used by some workers and the
autoregulation approach used by others in explaining the mechanisms of
hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
