It has been hypothesised that the 'set-point' for the long-term control of mean arterial (MAP) resides within the kidney. In this model, the set-point of the 'chronic renal function curve' establishes the steady state relationship between renal perfusion pressure and urinary excretion of sodium and water, which, in turn, affects blood volume and cardiac output. The 'renal-MAP set-point' theory predicts that the kidney controls MAP to maintain its own excretory function and that long-term regulation of blood volume and cardiac output are paramount to the regulation of arterial pressure. An alternative hypothesis is proposed in which the 'set-point' for the long-term control of MAP resides within the central nervous system (CNS) rather than the kidney. In contrast with the 'renal-MAP set-point' model, the 'CNS-MAP set-point' model dictates that the brain controls MAP to maintain cerebral blood flow and CNS function. The 'CNS-MAP set-point hypothesis' predicts that long-term regulation of MAP is paramount to the regulation of blood volume and cardiac output. It is proposed that the 'CNS-MAP set-point' system operates independently of the arterial baroreceptor reflex, which is a short-term controller of MAP. The precise mechanisms by which the CNS 'senses' MAP are complex and remain to be discovered. The MAP 'sensor' likely involves integration of hormone levels linked to body fluid homeostasis and osmoreceptor and baroreceptor inputs. It is also proposed that an as yet undiscovered 'central baroreceptor' exists within the brain itself. The 'CNS-MAP set-point hypothesis' predicts that many forms of experimental and essential hypertension are due to a primary shift in the CNS-MAP set-point.
|Original language||English (US)|
|Number of pages||10|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|State||Published - May 2005|
- Renal function curve
- Sympathetic nervous system