Evidence map›Paper›PMID 23224895›Full record

ArticleAdvances in experimental medicine and biology2013

Cross talk between plasma membrane Na(+)/Ca (2+) exchanger-1 and TRPC/Orai-containing channels: key players in arterial hypertension.

Maria V Pulina, A Zulian, Sergey G Baryshnikov, Cristina I Linde, Eiji Karashima, John M Hamlyn, Patrizia Ferrari, Mordecai P Blaustein, Vera A Golovina

Abstract read
In one paragraph

Article in Advances in experimental medicine and biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.4field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. NaAmerican journal of physiology. Heart and circulatory physiology · 2019
    Article
  10. Review
  11. Review
  12. Pivotal role of α2 NaThe Journal of physiology · 2016
    Review
  13. Endogenous Ouabain: Recent Advances and Controversies.Hypertension (Dallas, Tex. : 1979) · 2016
    Review
  14. Article
  15. Na+/Ca2+ exchange and Na+/K+-ATPase in the heart.The Journal of physiology · 2015
    Review
  16. Why isn't endogenous ouabain more widely accepted?American journal of physiology. Heart and circulatory physiology · 2014
    Article
  17. Age-related autoregulatory dysfunction and cerebromicrovascular injury in mice with angiotensin II-induced hypertension.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Article
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

9 authors at 2 institutions in 2 countries.

Maria V PulinaDepartment of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
A Zulian
Sergey G Baryshnikov
Cristina I Linde
Eiji Karashima
John M Hamlyn
Patrizia Ferrari
Mordecai P Blaustein
Vera A Golovina
University of Maryland, Baltimore · USSigma Tau (Italy) · IT

Funding

Sympathetic Neurotransmitters and Ouabain HypertensionP01HL078870 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BLAUSTEIN, MORDECAI P · 2005 to 2009
$9.9M
CALCIUM AND SODIUM TRANSPORT IN VASCULAR SMOOTH MUSCLER01HL045215 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BLAUSTEIN, MORDECAI P, HAMLYN, JOHN · 1990 to 2012
$4.1M
NHLBI NIH HHS P01 HL078870NHLBI NIH HHS R01 HL045215
6 · The paper itself

Abstract

Arterial smooth muscle (ASM) Na(+)/Ca(2+) exchanger type 1 (NCX1) and TRPC/Orai-containing receptor/store-operated cation channels (ROC/SOC) are clustered with α2 Na(+) pumps in plasma membrane microdomains adjacent to the underlying junctional sarcoplasmic reticulum. This arrangement enables these transport proteins to function as integrated units to help regulate local Na(+) metabolism, Ca(2+) signaling, and arterial tone. They thus influence vascular resistance and blood pressure (BP). For instance, upregulation of NCX1 and TRPC6 has been implicated in the pathogenesis of high BP in several models of essential hypertension. The models include ouabain-induced hypertensive rats, Milan hypertensive rats, and Dahl salt-sensitive hypertensive rats, all of which exhibit elevated plasma ouabain levels. We suggest that these molecular mechanisms are key contributors to the increased vascular resistance ("whole body autoregulation") that elevates BP in essential hypertension. Enhanced expression and function of ASM NCX1 and TRPC/Orai1-containing channels in hypertension implies that these proteins are potential targets for pharmacological intervention.

Indexed as

Calcium SignalingAnimalsCalciumDisease Models, AnimalHumansHypertensionMuscle ProteinsMuscle, Smooth, VascularRatsRats, Inbred DahlSodiumSodium-Calcium ExchangerTRPC6 Cation ChannelTRPC Cation ChannelsCalciumMuscle ProteinsSodiumSodium-Calcium Exchangersodium-calcium exchanger 1TRPC6 Cation ChannelTRPC6 protein, humanTrpc6 protein, ratTRPC Cation Channels

Identifiers

PMID23224895
PMCPMC3857394
OpenAlexW1523182977

What OpenQuestion holds

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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.