Document Detail


A new conceptual paradigm for the haemodynamics of salt-sensitive hypertension: a mathematical modelling approach.
MedLine Citation:
PMID:  22890716     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A conceptually novel mathematical model of neurogenic angiotensin II-salt hypertension is developed and analysed. The model consists of a lumped parameter circulatory model with two parallel vascular beds; two distinct control mechanisms for both natriuresis and arterial resistances can be implemented, resulting in four versions of the model. In contrast with the classical Guyton-Coleman model (GC model) of hypertension, in the standard version of our new model natriuresis is assumed to be independent of arterial pressure and instead driven solely by sodium intake; arterial resistances are driven by increased sympathetic nervous system activity in response to the elevated plasma angiotensin II and increased salt intake (AngII-salt). We compare the standard version of our new model against a simplified Guyton-Coleman model in which natriuresis is a function of arterial pressure via the pressure-natriuresis mechanism, and arterial resistances are controlled via the whole-body autoregulation mechanism. We show that the simplified GC model and the new model correctly predict haemodynamic and renal excretory responses to induced changes in angiotensin II and sodium inputs. Importantly, the new model reproduces the pressure-natriuresis relationship--the correlation between arterial pressure and sodium excretion--despite the assumption of pressure-independent natriuresis. These results show that our model provides a conceptually new alternative to Guyton's theory without contradicting observed haemodynamic changes or pressure-natriuresis relationships. Furthermore, the new model supports the view that hypertension need not necessarily have a renal aetiology and that long-term arterial pressure could be determined by sympathetic nervous system activity without involving the renal sympathetic nerves.
Authors:
Viktoria A Averina; Hans G Othmer; Gregory D Fink; John W Osborn
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-08-13
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-03     Completed Date:  2013-05-17     Revised Date:  2013-12-05    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  5975-92     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / physiology*
Animals
Arterial Pressure / physiology
Computer Simulation
Hemodynamics
Hypertension* / etiology,  physiopathology
Kidney / physiology
Models, Biological*
Sodium / physiology*
Grant Support
ID/Acronym/Agency:
GM29123/GM/NIGMS NIH HHS; HL076312/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
11128-99-7/Angiotensin II; 9NEZ333N27/Sodium
Comments/Corrections
Comment In:
J Physiol. 2013 Jun 1;591(Pt 11):2965   [PMID:  23729798 ]
J Physiol. 2013 Jun 1;591(Pt 11):2963   [PMID:  23729797 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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