Logical Issues With the Pressure Natriuresis Theory of Chronic Hypertension
Open accessAbstract
The term “abnormal pressure natriuresis” refers to a subnormal effect of a given level of blood pressure (BP) on sodium excretion. It is widely believed that abnormal pressure natriuresis causes an initial increase in BP to be sustained. We refer to this view as the “pressure natriuresis theory of chronic hypertension.” The proponents of the theory contend that all forms of chronic hypertension are sustained by abnormal pressure natriuresis, irrespective of how hypertension is initiated. This theory would appear to follow from “the three laws of long-term arterial pressure regulation” stated by Guyton and Coleman more than 3 decades ago. These “laws” articulate the concept that for a given level of salt intake, the relationship between arterial pressure and sodium excretion determines the chronic level of BP. Here, we review and examine the recent assertion by Beard that these “laws” of long-term BP control amount to nothing more than a series of tautologies. Our analysis supports Beard’s assertion, and also indicates that contemporary investigators often use tautological reasoning in support of the pressure natriuresis theory of chronic hypertension. Although the theory itself is not a tautology, it does not appear to be testable because it holds that abnormal pressure natriuresis causes salt-induced hypertension to be sustained through abnormal increases in cardiac output that are too small to be detected.
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The Guytonian view that the pressure-natriuresis relationship dominantly determines chronic blood pressure appears to express the three tautological laws of long-term arterial pressure regulation stated by Guyton and Coleman.
“It should also be noted that the Guytonian view on the dominant role of the pressure-natriuresis relationship in determining the chronic level of blood pressure, appears to be an expression of the three tautological “laws of long-term arterial pressure regulation” stated by Guyton and Coleman many years ago.39–42”
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 [41]
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- Authors
- Kurtz, T. W., DiCarlo, S. E., & Morris, R. C.
- Affiliations
- University of California, San Francisco (US)
- Wayne State University (US)
- Venue
- American Journal of Hypertension
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-11-08
- Volume
- 29
- Issue
- 12
- Pages
- 1325-1331
- ISSN
- 0895-7061 (ISSN-L)
- 1941-7225
- PMC
- PMC5353574
- OpenAlex
- W2586724690
- Semantic Scholar
- 162d981c880cff0cad18bd46000a772aaa846742
- Cited by
- 21
- References
- 44
- Citations by year
- 2026: 2 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 3 · 2017: 6 · 2016: 1
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Hypertension (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (5m01rr000079-42)
- National Heart, Lung, and Blood Institute (R01HL064230)
- National Center for Research Resources (M01-RR000079)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- pressure natriuresis, chronic hypertension, sodium excretion, blood pressure regulation, tautology, salt-induced hypertension, cardiac output, salt intake, hypertension pathophysiology
- MeSH terms
- Animals, Blood Pressure, Chronic Disease, Humans, Hypertension, Natriuresis, Pressure
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