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The CNS‐MAP‐Controller hypothesis: A new mathematical model for long‐term control of mean arterial pressure (MAP)
Author(s) -
Averina Viktoria,
Othmer Hans,
Fink Gregory,
Osborn John W
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1207.1
Subject(s) - hemodynamics , autoregulation , renal circulation , mean arterial pressure , medicine , renal function , blood pressure , kidney , neuroscience , cardiology , renal blood flow , psychology , heart rate
We present a new mathematical model in which the long‐term control of MAP is dominated by the central nervous system (CNS). The circulation is modeled as 2 parallel vascular beds; “renal” and “non‐renal”. The model assumes kidney function which fully adapts to chronic changes in MAP. The output of the “CNS‐MAP Controller” regulates sympathetic nerve activity (SNA) to renal and non‐renal arteriolar resistances and venous unstressed volume. Currently, the excitatory drive of the CNS‐MAP‐Controller consists of a synergistic interaction of circulating mineralocorticoids and plasma sodium. The model does not include primary renal dysfunction or “whole body autoregulation” as proposed in the Guyton‐Coleman model. Also, in contrast to the Guyton‐Coleman model in which one hemodynamic profile is proposed to underlie all forms of hypertension, our model suggests that several hemodynamic profiles associated with increased SNA are possible with either no change or decreased total blood volume. These hemodynamic profiles are consistent with published hemodynamic studies in experimental and human essential hypertension. This model supports the hypothesis that dysregulation in the brain, rather than kidney, can be responsible for the pathogenesis of hypertension. Supported by NIH Grant HL064178