ABSTRACT
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.
Subject(s)
Aldosterone/blood , Cholesterol/blood , Coronary Artery Disease/blood , Homocysteine/blood , Thrombosis/blood , Adrenal Glands/drug effects , Adrenal Glands/metabolism , Aged , Aldosterone/pharmacology , Animals , Arachidonic Acid/metabolism , Collagen/metabolism , Creatinine/blood , Female , Homocysteine/biosynthesis , Humans , In Vitro Techniques , Male , Middle Aged , Platelet Aggregation/drug effects , Rats , Rats, Sprague-Dawley , Sulfhydryl Compounds/bloodABSTRACT
The pathogenesis of liver damage in the course of hepatitis B virus (HBV) infection depends on the host's specific and non-specific immune response to various viral antigens. The role of polymorphonuclear neutrophils (PMN) in the natural immune reaction and during secondary microbial infections is well documented. Increased free radical production is associated with many pathological conditions such as shock, ischaemia or chronic inflammatory diseases. We studied the oxidative metabolism of neutrophils in patients with chronic HBV and after recovery (convalescents). The effect of the PreS1 fragment of HBV antigen on some neutrophil functions in vitro was also examined. There were significant differences in the values of spontaneous and stimulated oxidative burst of neutrophils, measured using luminol-chemiluminescence, in patients with HBV when compared with the convalescents. PreS1 antigen did not by itself induce the respiratory burst in human neutrophils but it potentiated their response to a second stimulus. Hence we observed a priming of neutrophils, for an enhanced respiratory burst, by PreS1 antigen.
Subject(s)
Hepatitis B Surface Antigens/immunology , Hepatitis B virus/immunology , Hepatitis B/virology , Neutrophils/immunology , Protein Precursors/immunology , Respiratory Burst , Viral Envelope Proteins/immunology , Adult , Aged , Cells, Cultured , Chronic Disease , Convalescence , Female , Hepatitis B Surface Antigens/pharmacology , Humans , Hydrogen Peroxide/immunology , Luminescent Measurements , Male , Middle Aged , Neutrophils/cytology , Protein Precursors/pharmacology , Viral Envelope Proteins/pharmacologyABSTRACT
The study was designed to study the effect of pentoxifylline PTX on the chemiluminescence responses of neutrophils and on tumor necrosis factor-alpha (TNF-alpha)-induced priming of neutrophils. The results demonstrate that TNF-alpha stimulated the respiratory burst by neutrophils and primed them for enhanced response to fMLP but not to PMA. The effect of TNF-alpha on the oxygen metabolism of neutrophils was inhibited when cells were treated with PTX. This reaction was dose-dependent. Additionally, the inhibiting influence of PTX on the chemiluminescence response of neutrophils was observed.
