Aldosterone modulates blood homocysteine and cholesterol in coronary artery disease patients: a possible impact on atherothrombosis?

Title:

Aldosterone modulates blood homocysteine and cholesterol in coronary artery disease patients: a possible impact on atherothrombosis?

Creator:

Karolczak, K, Kubalczyk, P, Watala, C, Pietruszynski, R, and Glowacki, R

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a00a55fd-6555-45f6-90db-b336a91c4cdc
uuid:a00a55fd-6555-45f6-90db-b336a91c4cdc
issn:0862-8408

Subject:

fyziologie člověka, human physiology, Platelet aggregation, Aldosterone, Atherosclerosis, Metabolism, Cardiovascular risk factors, Homocysteine, Cholesterol, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

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., K. Karolczak, P. Kubalczyk, R. Glowacki, R. Pietruszynski, C. Watala., and Seznam literatury

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:2

Harvested from:

CDK

Metadata only:

false