Evidence map›Paper›PMID 18443753›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2008

Signalling across the blood brain barrier by angiotensin II: novel implications for neurogenic hypertension.

Julian F R Paton, Sheng Wang, Jaimie W Polson, Sergey Kasparov

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

47 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. GABA is a mediator of brain ATHypertension research : official journal of the Japanese Society of Hypertension · 2020
    Review
  10. Review
  11. Article
  12. Article
  13. The Renin-Angiotensin System and Skeletal Muscle.Exercise and sport sciences reviews · 2018
    Review
  14. Article
  15. Review
  16. Hypothalamic and inflammatory basis of hypertension.Clinical science (London, England : 1979) · 2017
    Review
  17. Article
  18. Article
  19. Neuroinflammatory and autonomic mechanisms in diabetes and hypertension.American journal of physiology. Endocrinology and metabolism · 2016
    Review
  20. 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

4 authors at 3 institutions in 2 countries.

Julian F R PatonDepartment of Physiology & Pharmacology, Bristol Heart Institute, School of Medical Sciences, University of Bristol, Bristol, UK. Julian.F.R.Paton@Bristol.ac.uk
Sheng Wang
Jaimie W Polson
Sergey Kasparov
University of Bristol · GBNIHR Bristol Cardiovascular Biomedical Research Unit · GBUniversity School · US

Funding

British Heart Foundation RG/07/006/23634
6 · The paper itself

Abstract

Angiotensin II (AngII) is a major culprit in essential hypertension. Based on a genetic rodent model of hypertension, we review here evidence that AngII may signal across the blood brain barrier to affect neuronal circuits within the nucleus tractus solitarii (NTS) of the brainstem, a pivotal region regulating both the baroreceptor reflex and set point control of arterial pressure. We have termed this form of signalling as vascular-neuronal signalling. We describe that the depressant action of AngII in NTS on the baroreceptor reflex is mediated via activation of endothelial nitric oxide synthase (eNOS) releasing NO that promotes release of the inhibitory transmitter-GABA. This could shunt the incoming excitatory baroreceptor afferent traffic impinging on NTS neurones. Chronic studies recording arterial pressure in conscious unrestrained rats using radio-telemetry have revealed that eNOS in NTS plays an endogenous physiological role in the homeostatic regulation of the gain of the cardiac baroreceptor reflex. However, in the spontaneously hypertensive rat, eNOS mRNA was higher (compared to normotensive rats), and its chronic blockade in NTS restored the abnormally depressed cardiac baroreceptor reflex to levels akin to normotensive rats, improved heart rate variability and lowered arterial pressure. Hence, it seems that excessive eNOS activity in NTS of the SHR contributes to the pathological state of this animal model's cardiovascular autonomic nervous system. We speculate on why eNOS activity may be up regulated in the NTS of the SHR and propose that it is a consequence of high cerebral vascular resistance and inadequate blood perfusion of the brainstem.

Indexed as

Signal TransductionAngiotensin IIAnimalsBaroreflexBlood-Brain BarrierHumansHypertensionSolitary NucleusAngiotensin II

Identifiers

PMID18443753
OpenAlexW2163824042

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.