ArticleThe International journal of angiology : official publication of the International College of Angiology, Inc2007
Interaction between the heme oxygenase system and aldosterone in hypertension.
Article in The International journal of angiology : official publication of the International College of Angiology, Inc, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- Role of heme oxygenase in inflammation, insulin-signalling, diabetes and obesity.Mediators of inflammation · 2010Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chronic intraperitoneal administration of the heme oxygenase inducer, hemin (15 mg/kg daily), for three weeks reduced blood pressure in adult spontaneously hypertensive rats (SHR) from 210.1±1.03 mmHg to 127±0.9 mmHg (n=10, P<0.01) but had no effect on age-matched normotensive Wistar-Kyoto or Sprague-Dawley strains. The antihypertensive effect of hemin was accompanied by reduced expression of aldosterone synthase messenger RNA and depleted levels of plasma aldosterone (675.7±121.6 pg/mL versus 365.7±37 pg/mL; n=4, P<0.05).Because aldosterone is known to stimulate phospholipase C (PLC), the effect of hemin on PLC was examined. Hemin abated PLC activity (29.6±1.5 nmol/min/mL versus 3.1±0.9 nmol/min/mL; n=5, P<0.01) and this was accompanied by depleted levels of intracellular calcium (551±46 nM versus 103.2±6.3 nM; n=4, P<0.01) in the aorta of SHR. In contrast, enhanced heme oxygenase activity and elevated cyclic GMP levels (17.74±0.08 pmol/mg versus 30.4±2.3 pmol/mg protein; n=6, P<0.01) were detected in hemin-treated SHR. Additionally, hemin therapy also suppressed inflammatory and oxidative insults by significantly reducing nuclear factor kappa B messenger RNA expression while enhancing the total antioxidant capacity (0.22±0.02 Trolox equivalent antioxidant capacity (TEA C)/mg protein versus 0.60±0.04 TEA C/mg protein; n=4, P<0.01).The concomitant depletion of aldosterone, PLC activity, intracellular calcium and the corresponding decline of inflammatory and oxidative insults may account for the antihypertensive effects of hemin.
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Registered trials
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