Evidence map›Paper›PMID 18006579›Full record

ReviewThe Journal of physiology2008

Natriuretic peptide C receptor signalling in the heart and vasculature.

Robert A Rose, Wayne R Giles

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.

  1. Blood pressure loci identified with a gene-centric array.American journal of human genetics · 2011
    Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Biomarkers of Cardiovascular Stress: A Historical Review.Journal of cardiovascular development and disease · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia.International journal of molecular sciences · 2023
    Review
  14. The Natriuretic Peptide System: A Single Entity, Pleiotropic Effects.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Role of Cardiac Natriuretic Peptides in Heart Structure and Function.International journal of molecular sciences · 2022
    Review
  20. Article

23 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Robert A RoseDepartments of Physiology, Heart and Stroke/Richard Lewar Centre, University of Toronto and University Health Network, Toronto, Ontario, Canada M5S 3E2. rob.rose@utoronto.ca
Wayne R Giles
University of Calgary · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natriuretic peptides (NPs), including atrial, brain and C-type natriuretic peptides (ANP, BNP and CNP), bind two classes of cell surface receptors: the guanylyl cyclase-linked A and B receptors (NPR-A and NPR-B) and the C receptor (NPR-C). The biological effects of NPs have been mainly attributed to changes in intracellular cGMP following their binding to NPR-A and NPR-B. NPR-C does not include a guanylyl cyclase domain. It has been denoted as a clearance receptor and is thought to bind and internalize NPs for ultimate degradation. However, a substantial body of biochemical work has demonstrated the ability of NPR-C to couple to inhibitory G proteins (Gi) and cause inhibition of adenylyl cyclase and activation of phospholipase-C. Recently, novel physiological effects of NPs, mediated specifically by NPR-C, have been discovered in the heart and vasculature. We have described the ability of CNP, acting via NPR-C, to selectively inhibit L-type calcium currents in atrial and ventricular myocytes, as well as in pacemaker cells (sinoatrial node myocytes). In contrast, our studies of the electrophysiological effects of CNP on cardiac fibroblasts demonstrated an NPR-C-Gi-phospholipase-C-dependent activation of a non-selective cation current mediated by transient receptor potential (TRP) channels. It is also known that CNP and BNP have important anti-proliferative effects in cardiac fibroblasts that appear to involve NPR-C. In the mammalian resistance vessels, including mesenteric and coronary arteries, CNP has been found to function as an NPR-C-dependent endothelium-derived hyperpolarizing factor that regulates local blood flow and systemic blood pressure by hyperpolarizing smooth muscle cells. In this review we highlight the role of NPR-C in mediating these NP effects in myocytes and fibroblasts from the heart as well as in vascular smooth muscle cells.

Indexed as

Cardiovascular Physiological PhenomenaAnimalsBiological FactorsFibroblastsHumansMuscle, Smooth, VascularMyocytes, CardiacReceptors, Atrial Natriuretic FactorSignal Transductionatrial natriuretic factor receptor CBiological Factorsendothelium-dependent hyperpolarization factorReceptors, Atrial Natriuretic Factor

Identifiers

PMID18006579
PMCPMC2375602
OpenAlexW1584351787

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.