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
Many mammalian species including human are immature at birth and undergo major developmental changes during suckling and weaning period. This problem is also conspicuous for the gastrointestinal tract that undergoes abrupt transitions coinciding with birth and weaning. This review deals with the maturation of ion transport functions in colon,
the intestinal segment that plays an important role in sodium and potassium absorption and secretion. The purpose of the present review is to summarize the mechanism of sodium and potassium transport pathways and show how these transport processes change postnatally and how hormones, particularly corticosteroids, modify the pattern of
development. Finally we describe some of the ways, how to analyze corticosteroid metabolism in target tissue.
Metabolic acidosis could occur due to either endogenousm acids accumulation or bicarbonate loss from the gastrointestinal tract or commonly from the kidney. This study aimed to investigatethe possible underlying mechanism(s) of chronic acidosis-inducedcardiac contractile and electrical
changes in rats. Twenty four adult Wistar rats, of both sexes, were randomly divided into control group and chronic metabolic acidosis group, which received orally 0.28 M NH4Cl in the drinking water for 2 weeks. At
the end of experimental period, systolic and diastolic blood pressure values
were measured. On the day of sacrifice, rats were an esthetized by i.p. pentobarbitone (40mg/kg b.w.), transthoracic echocardiography and ECG
were performed. Blood samples were obtained from abdominal aorta for complete blood count and determination of pH, bicarbonate, chloride,
sodium, potassium, troponin I, CK-MB, IL-6, renin and aldosterone levels.
Hearts from both groups were studied for cardiac tissue IL-6 and
aldosterone in addition to histopathological examination.
Compared to control group, chronic metabolic acidosis groupshowed anemia, significant systolic and diastolic hypotension accompanied by significant reduction of ejection fraction and fraction of shortening, significant bradycardia, prolonged QTc interval and higher widened T wave
as well as significantly elevated plasma levels of renin, aldosterone, troponin
I, CK-MB and IL-6, and cardiac tissue aldosterone and IL-6. The left
ventricular wall of the acidosis group showed degenerated myocytes
with fibrosis and apoptosis. Thus, chronic metabolic acidosis induced negative inotropic and chronotropic effects and cardiomyopathy, possibly by elevated aldosterone and IL-6 levels released from the cardiac tissue.