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Cited by 117Renin-Angiotensin System StudiesBlood Pressure and Hypertension StudiesEicosanoids and Hypertension Pharmacology

Mechanisms of pressure natriuresis

Granger, Joey P., Alexander, Barbara T., Llinas, Mayte·2002·Current Hypertension Reports
DOI 10.1007/s11906-002-0040-3
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Abstract

A central component of the feedback system for long-term control of arterial pressure is the pressure-natriuresis mechanism, whereby increases in renal perfusion pressure lead to decreases in sodium reabsorption and increases in sodium excretion. The specific intrarenal mechanism for the decrease in tubular reabsorption in response to increases in renal perfusion pressure appears to be related to increases in hemodynamic factors such as medullary blood flow and renal interstitial hydrostatic pressure (RIHP), and renal autocoids such as nitric oxide, prostaglandins, kinins, and angiotensin II. Increases in renal perfusion pressure are associated with significant increases in RIHP, nitric oxide, prostaglandin E2, and kinins, and decreases in angiotensin II. The mechanism whereby RIHP increases in the absence of discernible changes in whole kidney renal blood flow and peritubular capillary hydrostatic and/or oncotic pressures may be related to increases in renal medullary flow as a result of nitric oxide-induced reductions in renal medullary vascular resistance. Several lines of investigation support an important quantitative role for RIHP in mediating pressure natriuresis. Preventing RIHP from increasing in response to increases in renal perfusion pressure markedly attenuates pressure natriuresis. Furthermore, direct increases in RIHP, comparable to increases measured in response to increases in renal perfusion pressure, have been shown to significantly decrease tubular reabsorption of sodium in the proximal tubule and increase sodium excretion. The exact mechanism whereby RIHP influences tubular reabsorption is unknown, but may be related to alterations in tight junctional permeability to sodium in proximal tubules, redistribution of apical sodium transporters, and/or release of renal autacoids such as prostaglandin E2.

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Authors
Granger, J. P., Alexander, B. T., & Llinas, M.
Affiliations
University of Mississippi Medical Center (US)
ORCID
Venue
Current Hypertension Reports
Publisher
Springer Science and Business Media LLC
Published
2002-03
Volume
4
Issue
2
Pages
152-159
ISSN
  • 1522-6417 (ISSN-L)
  • 1534-3111
DOI
10.1007/s11906-002-0040-3
OpenAlex
W2077120585
Cited by
117
References
63
Citations by year
2026: 2 · 2025: 2 · 2024: 8 · 2023: 7 · 2022: 4 · 2021: 6 · 2020: 1 · 2019: 3 · 2018: 8 · 2017: 7 · 2016: 2 · 2015: 3 · 2014: 7 · 2013: 4 · 2012: 10
FWCI
2.85
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Current Hypertension Reports (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL10137-01, HL-38499, HL‐51971, P01HL051971, F32HL010137)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
pressure natriuresis, renal perfusion pressure, renal interstitial hydrostatic pressure, sodium reabsorption, sodium excretion, renal medullary blood flow, nitric oxide, prostaglandin E2, kinins, angiotensin II, proximal tubule, blood pressure regulation
MeSH terms
Blood Pressure, Hemodynamics, Humans, Hydrostatic Pressure, Hypertension, Renal, Kidney, Natriuresis, Nephrons, Renal Circulation, Sodium

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