ArticleEndocrinology2018
Effect of Angiotensin II and ACTH on Adrenal Blood Flow in the Male Rat Adrenal Gland In Vivo.
Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Adrenal Hemorrhaging in a Patient with Severe Obstructive Sleep Apnea Syndrome with Elevated Plasma ACTH Levels.Internal medicine (Tokyo, Japan) · 2023Article
- Salt-Sensitive Hypertension in GRInternational journal of molecular sciences · 2021Article
- Treatment of Primary Aldosteronism Increases Plasma Epoxyeicosatrienoic Acids.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Non-Canonical Effects of ACTH: Insights Into Adrenal Insufficiency.Frontiers in endocrinology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Angiotensin II (Ang II) and adrenocorticotropic hormone (ACTH) regulate adrenal vascular tone in vitro through endothelial and zona glomerulosa cell-derived mediators. The role of these mediators in regulating adrenal blood flow (ABF) and mean arterial pressure (MAP) was examined in anesthetized rats. Ang II (0.01 to 100 ng/kg) increased ABF [maximal increase of 97.2 ± 6.9 perfusion units (PUs) at 100 ng/kg] and MAP (basal, 115 ± 7 mm Hg; Ang II, 163 ± 5 mm Hg). ACTH (0.1 to 1000 ng/kg) also increased ABF (maximum increase of 91.4 ± 10.7 PU) without changing MAP. ABF increase by Ang II was partially inhibited by the nitric oxide (NO) synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME) (maximum increase of 72.9 ± 4.2 PU), the cytochrome P450 inhibitor miconazole (maximum increase of 39.1 ± 6.8 PU) and the epoxyeicosatrienoic acid (EET) antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) (maximum increase of 56.0 ± 13.7 PU) alone, whereas combined administration of miconazole and L-NAME (maximum increase of 16.40 ± 8.98 PU) ablated it. These treatments had no effect on MAP. Indomethacin did not affect the increase in ABF or MAP induced by Ang II. The ABF increase by ACTH was partially ablated by miconazole and 14,15-EEZE but not by L-NAME. Steroidogenic stimuli such as Ang II and ACTH increase ABF to promote oxygen and cholesterol delivery for steroidogenesis and aldosterone transport to its target tissues. The increases in ABF induced by Ang II are mediated by release of NO and EETs, whereas ABF increases with ACTH are mediated by EETs only.
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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.