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EN
Atrial myocytes synthesise atrial natriuretic factor prohormone consisting of 126 aminoacids (ANP1-126 ) which is subsequently processes to several fragments. Atrial natriuretic factor (ANF, ANP99-126) originating from the C-terminal portion of prohormone is a best described atrial peptide. However, several peptides originating from the N-terminus of this precursor also circulate and produce significant diuresis, natriuresis and vasodilatation. These are: long acting natriuretic peptide (ANP1-30), vessel dilator (ANP31-67) and kaliuretic peptide (ANP79-98). ANP1-98 and ANP68-98 also circulate. Kaliuretic peptide specifically stimulates urinary potassium excretion. These peptides are slowly metabolised and their plasma concentration is higher than ANF suggesting their important role in water-electrolyte homeostasis and regulation of vascular tone. N-terminal atrial peptides don?t bind to classical natriuretic peptide receptors, each of them has probably its own unique receptors. Although these peptides activate particulate guanylate cyclase in a number of tissues, some of their effects, for example natriuresis, are not mediated by cGMP but rather by prostaglandin E2. Plasma concentration of N-terminal atrial peptides may be useful in diagnosis and risk stratification in patients with heart failure and after myocardial infarction. Recently N-terminal fragment of brain natriuretic peptide (BNP1-76) was identified in the blood. This peptide is secreted together with its C-terminal partner, BNP77-108 by ventricular myocytes. Some studies that N-terminal BNP may be also a useful diagnostic tool in cardiovascular diseases.
EN
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear receptors which regulate the expression of target genes. Three types of PPAR have been identified: PPAR alpha, PPAR beta/delta and PPAR gamma. The known endogenous PPAR ligands are polyunsaturated fatty acids and eicosanoids, such as 15-deoxy-delta12,14-prostaglandin J2 and leukotriene B4. Two classes of drugs, fibrates and thiazolidinediones bind to PPAR alpha and PPAR gamma, respectively. PPARs are involved in the regulation of the lipid metabolism and adipogenesis but are also expressed in the vasculature. PPARs activators inhibit inflammatory reactions within the vascular wall, inhibit vascular smooth muscle cells migration and proliferation and affect foam cells formation by changing the expression different animal models of hypertension as well as in humans. PPAR gamma ligands inhibit the development of atherosclerosis in LDL receptor deficient and apolipoprotein E deficient mice and in diabetic humans. PPARgamma agonists have also been shown to attenuate myocardial hypertrophy and protect against ischemia-reperfusion injury.
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