Evidence map›Paper›PMID 9202051›Full record

ArticleThe Journal of clinical investigation1997

Kallistatin is a potent new vasodilator.

J Chao, J N Stallone, Y M Liang, L M Chen, D Z Wang, L Chao

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 92 citations in OpenAlex.

  1. Kallistatin levels in HIV-infected patients and effects of statin therapy.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2017
    Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Kallistatin inhibits lymphangiogenesis and lymphatic metastasis of gastric cancer by downregulating VEGF-C expression and secretion.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2018
    Article
  7. Article
  8. Review
  9. Observational
  10. Review
  11. Protective Role of Kallistatin in Vascular and Organ Injury.Hypertension (Dallas, Tex. : 1979) · 2016
    Review
  12. Nafamostat mesilate promotes endothelium-dependent vasorelaxation via the Akt-eNOS dependent pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  13. Review
  14. Article
  15. Article
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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

6 authors at 2 institutions in 1 country.

J ChaoDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
J N Stallone
Y M Liang
L M Chen
D Z Wang
L Chao
Medical University of South Carolina · USNortheast Ohio Medical University · US

Funding

Regulation and Function of Tissue KallikreinR01HL029397 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1986 to 2012
$3.9M
RENAL KALLIKREIN-BINDING PROTEIN IN HYPERTENSIONR01HL044083 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1990 to 2008
$2.1M
SEX DIMORPHISM IN VASCULAR FUNCTION--HUMORAL MECHANISMSR29HL047432 · NHLBI · TEXAS A&M UNIVERSITY SYSTEM · PI STALLONE, JOHN NICHOLAS · 1993 to 1997
–
NHLBI NIH HHS HL-29397NHLBI NIH HHS HL-44083NHLBI NIH HHS HL-47432
6 · The paper itself

Abstract

Kallistatin is a serine proteinase inhibitor which binds to tissue kallikrein and inhibits its activity. The aim of this study is to evaluate if kallistatin has a direct effect on the vasculature and on blood pressure homeostasis. We found that an intravenous bolus injection of human kallistatin caused a rapid, potent, and transient reduction of mean arterial blood pressure in anesthetized rats. Infusion of purified kallistatin (0.07-1.42 nmol/kg) into cannulated rat jugular vein produced a 20-85 mmHg reduction of blood pressure in a dose-dependent manner. Hoe 140, a bradykinin B2-receptor antagonist, had no effect on the hypotensive effect of kallistatin yet it abolished the blood pressure-lowering effect of kinin and kallikrein. Relaxation of isolated aortic rings by kallistatin was observed in the presence (ED50 of 3.4 x 10(-9) M) and in the absence of endothelium (ED50 of 10(-9) M). Rat kallikrein-binding protein, but not kinin or kallikrein, induced vascular relaxation of aortic rings. Neither Hoe 140 nor Nomega-nitro--arginine methyl ester, a nitric oxide synthase inhibitor, affected vasorelaxation induced by kallistatin. Kallistatin also caused dose-dependent vasodilation of the renal vasculature in the isolated, perfused rat kidney. Specific kallistatin-binding sites were identified in rat aorta by Scatchard plot analysis with a Kd of 0.25+/-0.07 nM and maximal binding capacity of 47.9+/-10.4 fmol/mg protein (mean+/-SEM, n = 3). These results indicate that kallistatin is a potent vasodilator which may function directly through a vascular smooth muscle mechanism independent of an endothelial bradykinin receptor. This study introduces the potential significance of kallistatin in directly regulating blood pressure to reduce hypertension.

Indexed as

Vasodilator AgentsAdrenergic beta-AntagonistsAnimalsAorta, ThoracicBlood PressureBradykininCarrier ProteinsHumansInfusions, IntravenousInjections, IntravenousIn Vitro TechniquesKallikreinsKininsMaleMembrane ProteinsMuscle ContractionAdrenergic beta-AntagonistsBradykininCarrier ProteinsicatibantKallikreinskallistatinKininsMembrane ProteinsNG-Nitroarginine Methyl EsterSerpinsVasodilator Agents

Identifiers

PMID9202051
PMCPMC508159
OpenAlexW2055104787

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.