Aldosterone modulates blood homocysteine and cholesterol in coronary artery disease patients - a possible impact on atherothrombosis?
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
29303611
DOI
10.33549/physiolres.933668
PII: 933668
Knihovny.cz E-resources
- MeSH
- Platelet Aggregation drug effects MeSH
- Aldosterone blood pharmacology MeSH
- Cholesterol blood MeSH
- Homocysteine biosynthesis blood MeSH
- Collagen metabolism MeSH
- Creatinine blood MeSH
- Rats MeSH
- Arachidonic Acid metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Adrenal Glands drug effects metabolism MeSH
- Coronary Artery Disease blood MeSH
- Rats, Sprague-Dawley MeSH
- Aged MeSH
- Sulfhydryl Compounds blood MeSH
- In Vitro Techniques MeSH
- Thrombosis blood MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Aldosterone MeSH
- Cholesterol MeSH
- Homocysteine MeSH
- Collagen MeSH
- Creatinine MeSH
- Arachidonic Acid MeSH
- Sulfhydryl Compounds MeSH
Aldosterone plays a key role in maintaining the homeostasis of the whole organism. Under some circumstances, aldosterone can contribute to the progression of cardiovascular diseases, including coronary artery disease. This study demonstrates that aldosterone associates negatively with some lipidogram parameters and positively with the concentration of homocysteine. These associations are characteristic for coronary artery disease and are not present in control subjects. The findings also indicate that in vitro aldosterone stimulates homocysteine production by rat adrenal glands, which may explain the associations observed with coronary artery disease. Moreover, we have found that aldosterone significantly modulates in vitro platelet reactivity to arachidonate and collagen - aldosterone increases the pro-aggregatory action of collagen, but decreases the pro-aggregatory potential of arachidonate. Therefore, the findings of these in vitro and ex vivo experiments indicate the existence of new pathways by which aldosterone modulates lipid- homocysteine- and platelet-dependent atherogenesis.
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