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Cited by 54Blood Pressure and Hypertension StudiesRenin-Angiotensin System StudiesHeart Rate Variability and Autonomic Control

Current computational models do not reveal the importance of the nervous system in long‐term control of arterial pressure

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Osborn, John W., Averina, Viktoria A., Fink, Gregory D.·2009·Experimental Physiology
DOI 10.1113/expphysiol.2008.043281PMC PMC2684060
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Abstract

Arterial pressure is regulated over long periods of time by neural, hormonal and local control mechanisms, which ultimately determine the total blood volume and how it is distributed between the various vascular compartments of the circulation. A full understanding of the complex interplay of these mechanisms can be greatly facilitated by the use of mathematical models. In 1967, Guyton and Coleman published a model for long‐term control of arterial pressure that focused on renal control of body sodium and water and thus total blood volume. The central point of their model is that the long‐term level of arterial pressure is determined exclusively by the ‘renal function curve’, which relates arterial pressure to urinary excretion of salt and water. The contribution of the sympathetic nervous system to setting the long‐term level of arterial pressure in the model is limited. In light of the overwhelming evidence for a major role of the sympathetic nervous system in long‐term control of arterial pressure and the pathogenesis of hypertension, new mathematical models for long‐term control of arterial pressure may be necessary. Despite the prominence and general acceptance of the Guyton–Coleman model in the field of hypertension research, we argue here that it overestimates the importance of renal control of body fluids and total blood volume in blood pressure regulation. Furthermore, we suggest that it is possible to construct an alternative model in which sympathetic nervous system activity plays an important role in long‐term control of arterial pressure independent of its effects on total blood volume.

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  • The omission of the pressure-natriuresis relationship as a blood pressure driver in HumMod and other contemporary models aligns with Beard's warning to stop teaching and promoting physiologic concepts based on tautological thinking.

    “The omission of the pressure-natriuresis relationship as a driver of blood pressure outcomes in HumMod, and in other contemporary models,35–38 agrees with Beard’s admonition to stop teaching and promoting physiologic concepts that are based on tautological thinking.39”

    From Testing Computer Models Predicting Human Responses to a High-Salt Diet: Implications for Understanding Mechanisms of Salt-Sensitive Hypertension (2018) · cites this paper as [35]

    In “Establishment of a new mathematical model for long-term control of arterial pressure” (page unavailable), the authors reject pressure–natriuresis as an overriding determinant of long-term blood pressure. But they explicitly say their proposed model will include a pressure–natriuresis relationship, primarily as a back-up mechanism; the paper therefore does not support describing the relationship as omitted. Beard’s admonition has a separate citation in the citing sentence and is not assessed here. (LLM, conf=0.84)

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  • Osborn and colleagues and Beard and colleagues deliberately excluded the pressure-natriuresis curve as the main blood pressure controller in their modern arterial pressure models.

    “Further, Osborn and colleagues35–37 and Beard and colleagues38 pointedly chose not to include the pressure natriuresis curve as the main controller of blood pressure in their modern models of arterial pressure regulation.”

    From Testing Computer Models Predicting Human Responses to a High-Salt Diet: Implications for Understanding Mechanisms of Salt-Sensitive Hypertension (2018) · cites this paper as [35]

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Research works printed but not linked: 3

  1. Guyton AC Circulatory Physiology III: Arterial Pressure and Hypertension 1980 W. B. Saunders Co. Philadephia
  2. Guyton AC Coleman TG Long-term Regulation of the Circulation: Interrelationships with Body Fluid Volumes 1967 W. B. Saunders Co. Philadelphia
  3. Guyton AC Jones CE Coleman TG Circulatory Physiology: Cardiac Ouput and its Regulation 1973 W. B. Saunders Co. Philadelphia

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Authors
Osborn, J. W., Averina, V. A., & Fink, G. D.
Affiliations
  • University of Minnesota (US)
  • Michigan State University (US)
ORCID
Venue
Experimental Physiology
Publisher
Wiley
Published
2009-03-12
Volume
94
Issue
4
Pages
389-396
ISSN
  • 0958-0670 (ISSN-L)
  • 1469-445X
DOI
10.1113/expphysiol.2008.043281
PMC
PMC2684060
OpenAlex
W2167635127
Semantic Scholar
ed4b534cbab4e5c252a20091622b5b07f7ca51d3
Cited by
53
References
39
Citations by year
2026: 1 · 2022: 1 · 2021: 4 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 4 · 2014: 7 · 2013: 3 · 2012: 7
FWCI
5.61
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Experimental Physiology (publishedVersion, public-domain)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL116476, R01HL076312)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
Keywords
sympathetic nervous system, blood volume, hypertension pathogenesis
MeSH terms
Animals, Arteries, Blood Pressure, Blood Volume, Computer Simulation, Homeostasis, Humans, Hypertension, Kidney, Models, Cardiovascular, Natriuresis, Sympathetic Nervous System, Reproducibility of Results

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