Evidence map›Paper›PMID 9405684›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Genetically determined chloride-sensitive hypertension and stroke.

M Tanaka, O Schmidlin, S L Yi, A W Bollen, R C Morris

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Pendrin: linking acid base to blood pressure.Pflugers Archiv : European journal of physiology · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. SymbiosalEFSA journal. European Food Safety Authority · 2018
    Article
  7. Article
  8. Review
  9. Review
  10. The hidden hand of chloride in hypertension.Pflugers Archiv : European journal of physiology · 2015
    Review
  11. Overexpression of pendrin in intercalated cells produces chloride-sensitive hypertension.Journal of the American Society of Nephrology : JASN · 2013
    Article
  12. The role of the kidney in salt-sensitive hypertension.Clinical and experimental nephrology · 2012
    Review
  13. Claudin-4 forms paracellular chloride channel in the kidney and requires claudin-8 for tight junction localization.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  14. Article
  15. Article
  16. What effect does potassium have on blood pressure?Journal of clinical hypertension (Greenwich, Conn.) · 2008
    Article
  17. Sodium-selective salt sensitivity: its occurrence in blacks.Hypertension (Dallas, Tex. : 1979) · 2007
    Article
  18. Review
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

5 authors.

M TanakaDepartment of Medicine, General Clinical Research Center, University of California, 1202 Moffitt Hospital, San Francisco, CA 94143-0126, USA.
O Schmidlin
S L Yi
A W Bollen
R C Morris

Funding

ZD1839 FOR MALIGNANT ASTROCYTOMA OR GLIOBLASTOMA AND MENINGIOMAM01RR000079 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KESSLER, DAVID A · 1985 to 2006
$26.0M
DIETARY POTASSIUM AS A DETERMINANT OF HYPERTENSIONR01HL047943 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MORRIS, RALPH CURTIS · 1991 to 1994
–
NCRR NIH HHS 5 MO1 RR-000079NCRR NIH HHS M01 RR000079NHLBI NIH HHS R01 HL47943
6 · The paper itself

Abstract

The stroke-prone spontaneously hypertensive rat (SHRSP) is a genetically determined model of "salt-sensitive" stroke and hypertension whose full phenotypic expression is said to require a diet high in Na+ and low in K+. We tested the hypothesis that dietary Cl- determines the phenotypic expression of the SHRSP. In the SHRSP fed a normal NaCl diet, supplementing dietary K+ with KCl exacerbated hypertension, whereas supplementing either KHCO3 or potassium citrate (KB/C) attenuated hypertension, when blood pressure (BP) was measured radiotelemetrically, directly and continually. Supplemental KCl, but not KB/C, induced strokes, which occurred in all and only those rats in the highest quartiles of both BP and plasma renin activity (PRA). PRA was higher with KCl than with KB/C. These observations demonstrate that with respect to both severity of hypertension and frequency of stroke the phenotypic expression of the SHRSP is (i) either increased or decreased, depending on whether the anionic component of the potassium salt supplemented is, or is not, Cl-; (ii) increased by supplementing Cl- without supplementing Na+, and despite supplementing K+; and hence (iii) both selectively Cl--sensitive and Cl--determined. The observations suggest that in the SHRSP selectively supplemented with Cl- the likelihood of stroke depends on the extent to which both BP and PRA increase.

Indexed as

AnimalsCerebrovascular DisordersHypertensionRatsRats, Inbred SHRSodium Chloride, DietarySodium Chloride, Dietary

Identifiers

PMID9405684
PMCPMC25108

What OpenQuestion holds

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Registered trials

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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.