Evidence map›Paper›PMID 11884271›Full record

ReviewCurrent hypertension reports2002

Mechanisms of pressure natriuresis.

Joey P Granger, Barbara T Alexander, Mayte Llinas

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.5field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 119 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Complex equilibrium involving aldosterone underlies the pathophysiology of renovascular hypertension.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2025
    Article
  5. Observational
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  8. Review
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  14. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Joey P GrangerDepartment of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505, USA. jgranger@physiology.umsmed.edu
Barbara T Alexander
Mayte Llinas
Jackson Memorial Hospital · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI RECKELHOFF, JANE F · 1993 to 2018
$39.4M
ABNORMAL PRESSURE NATRIURESIS IN HYPERTENSIONR01HL038499 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI GRANGER, JOEY P. · 1989 to 2009
$1.4M
CARDIOVASCULAR/RENAL MECHANISMS OF HYPERTENSIONF32HL010137 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI ALEXANDER, BARBARA T · 1999 to 2001
$80k
ABNORMAL PRESSURE NATRIURESIS IN HYPERTENSIONR23HL038499 · NHLBI · EASTERN VIRGINIA MEDICAL SCHOOL · PI GRANGER, JOEY P. · 1986 to 1987
–
NHLBI NIH HHS HL 10137-01NHLBI NIH HHS HL 38499NHLBI NIH HHS HL 51971
6 · The paper itself

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.

Indexed as

Blood PressureHemodynamicsHumansHydrostatic PressureHypertension, RenalKidneyNatriuresisNephronsRenal CirculationSodiumSodium

Identifiers

PMID11884271
OpenAlexW2077120585

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.