Trial reportThe Journal of physiology2006
Angiotensin II: a major regulator of subcutaneous adipose tissue blood flow in humans.
Trial report in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The relationship between adipose tissue RAAS activity and the risk factors of prediabetes: a systematic review and meta-analysis.Adipocyte · 2023Pooled it
- Trial
- Bioengineered Pancreas-Liver Crosstalk in a Microfluidic Coculture Chip Identifies Human Metabolic Response Signatures in Prediabetic Hyperglycemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Measurement of human abdominal and femoral intravascular adipose tissue blood flow using percutaneous Doppler ultrasound.Adipocyte · 2021Article
- Adipocyte-Endothelium Crosstalk in Obesity.Frontiers in endocrinology · 2021Review
- Impact of high-fat diet on vasoconstrictor reactivity of white and brown adipose tissue resistance arteries.American journal of physiology. Heart and circulatory physiology · 2019Article
- Adipose tissue dysfunction and impaired metabolic health in human obesity: a matter of oxygen?Frontiers in endocrinology · 2015Review
- Regulation of human subcutaneous adipose tissue blood flow.International journal of obesity (2005) · 2014Review
- Review
- Regulation of stem cell differentiation in adipose tissue by chronic inflammation.Clinical and experimental pharmacology & physiology · 2011Review
- Adipose tissue vascularization: its role in chronic inflammation.Current diabetes reports · 2011Review
- Emerging role of adipose tissue hypoxia in obesity and insulin resistance.International journal of obesity (2005) · 2009Review
- Local adipose tissue renin-angiotensin system.Current hypertension reports · 2008Review
- Adipocytes do not significantly contribute to plasma angiotensinogen.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
We investigated the functional roles of circulating and locally produced angiotensin II (Ang II) in fasting and postprandial adipose tissue blood flow (ATBF) regulation and examined the interaction between Ang II and nitric oxide (NO) in ATBF regulation. Local effects of the pharmacological agents (or contralateral saline) on ATBF, measured with 133Xe wash-out, were assessed using the recently developed microinfusion technique. Fasting and postprandial (75 g glucose challenge) ATBF regulation was investigated in nine lean healthy subjects (age, 29 +/- 3 years; BMI, 23.4 +/- 0.7 kg m(-2)) using local Ang II stimulation, Ang II type 1 (AT1) receptor blockade, and angiotensin-converting enzyme (ACE) inhibition. Furthermore, NO synthase (NOS) blockade alone and in combination with AT1 receptor blockade was used to examine the interaction between Ang II and NO. Ang II induced a dose-dependent decrease in ATBF (10(-9)m: -16%, P = 0.04; 10(-7)m: -33%, P < 0.01; 10(-5)m: -53%P < 0.01). Fasting ATBF was not affected by ACE inhibition, but was increased by approximately 55% (P < 0.01) by AT(1) receptor blockade. NOS blockade induced a approximately 30% (P = 0.001) decrease in fasting ATBF. Combined AT1 receptor and NOS blockade increased ATBF by approximately 40% (P = 0.003). ACE inhibition and AT1 receptor blockade did not affect the postprandial increase in ATBF. We therefore conclude that circulating Ang II is a major regulator of fasting ATBF, and a major proportion of the Ang II-induced decrease in ATBF is NO independent. Locally produced Ang II does not appear to regulate ATBF. Ang II appears to have no major effect on the postprandial enhancement of ATBF.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.