A Steady-State Control Analysis of the Renin-Angiotensin-Aldosterone System
This communication develops a steady-state block diagram about the configuration of the renin-angiotensin-aldosterone system in relation to the mineralocorticoid-dependent reabsorption of sodium. Two principal mechanisms appear to be involved in the control of renin secretion. The baroreceptor hypothesis suggests that decreased stretch of the afferent glomerular arteriole produces increased renin secretion. The macula densa theory, on the other hand, suggests that renin secretion responds to alterations either in sodium load or in sodium concentration at the macula densa. These two receptors are presented as parallel feedback pathways which are independently capable of altering renin secretion. This concept of independent receptor function is supported by literature in which one of the receptor pathways was eliminated. The system configuration for the renin-angiotensin-aldosterone system suggests the hypothesis that the vascular receptor controls renin secretion in the autoregulatory range of blood pressure and that macula densa control dominates at pressures below the autoregulatory range. The control system diagram also calls attention to certain unique features of the renin-angiotensin-aldosterone system; it indicates that (1) a chronic low-sodium diet involves changes in both input variables (extracellular fluid volume) and parameters (hepatic blood flow) to maximize sodium reabsorption, (2) thoracic inferior vena cava constriction opens the feedback loop so that the renal receptors do not perceive increases in extracellular fluid volume, (3) congestive heart failure reduces the overall gain of the system, and (4) a small nonhypotensive hemorrhage primarily increases renin secretion through renal sympathetic nerve stimulation.
- sodium reabsorption
- renal baroreceptor hypothesis
- congestive heart failure
- renal autoregulation
- low-sodium diet
- constriction of thoracic vena cava
- macula densa receptor
- Received September 30, 1971.
- Accepted April 10, 1972.
- © 1972 American Heart Association, Inc.