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

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.

Mechanism of action of homocysteine and its thiolactone in hemostasis system.

In the article, the actions of homocysteine (Hcys) and its metabolite - cyclic thioester - homocysteine thiolactone (HTL) on complex process of hemostasis, which regulates the flowing properties of blood, are described. Possible interaction of Hcys and HTL with endothelial cells, blood platelets, plasmatic fibrinogen and plasminogen, as the important major components of hemostasis are also discussed. The modification of hemostatic proteins (N-homocysteinylated or S-homocysteinylated proteins) induced by Hcys or its thiolactone, and links of homocysteine or homocysteine thiolactone to "NO metabolism seem to be the main reason of biotoxicty of homocysteine in cardiovascular diseases.

The effects of methylprednisolone and mitoxantrone on CCL5-induced migration of lymphocytes in multiple sclerosis.

OBJECTIVES: Chemokines are involved in migration of inflammatory cells to the central nervous system (CNS) in multiple sclerosis (MS). The aim of this study was the analysis of the impact of MS treatment on CCL5-induced migration of leukocyte subpopulations. MATERIAL AND METHODS: Migration of lymphocytes and monocytes from blood of MS patients treated with methylprednisolone (MP) or mitoxantrone (MTX) was analysed in a chemotaxis chamber. RESULTS: CCL5-induced migration of lymphocytes from untreated MS patients was significantly increased over controls. The treatment of MS with MP and MTX reduced this chemotaxis. The plasma level of CCL5 was increased in MS patients before treatment and was also significantly decreased in the treatment of MS with MP and MTX. CONCLUSIONS: This observation supports the hypothesis that in MS, chemokine CCL5 may induce migration of leukocytes to the CNS and suggests that treatment of the disease with MP and MTX may reduce this migration.