The impact of cardiorenal syndrome on vascular ectonucleotidases

Abstract

Cardiorenal Syndrome (CRS) is defined as an acute or chronic dysfunction of the heart and kidneys, in which injury to one organ causes disturbances in the other. The vascular system is also affected by this syndrome through hemodynamic, mechanical, biochemical, neurohumoral, and protein-bound uremic toxins. The purinergic system exerts its signaling through extracellular nucleotides and nucleosides that bind the purinergic receptors to trigger a response, having great importance in cardiovascular regulation, mediating several biological processes, including vasodilation, vasoconstriction, and inflammation. Ectonucleotidases are enzymes that regulate the concentration and activity of nucleotides and nucleosides in the extracellular environment, catabolizing them and ceasing their action. Extracellular ATP can function as DAMP (damage-associated molecular pattern), stimulating an inflammatory response and promoting injury, but it can also contribute to tissue repair. Adenosine, in turn, is recognized for its anti-inflammatory action. Thereby, it is important to regulate the availability of these molecules. This project highlights the main ectonucleotidases present in the vasculature: NTPDase1, NTPDase2 and ecto-5'-nucleotidase, aiming to analyze possible changes in the gene expression of these enzymes in the aorta of mice submitted to renal ischemia and reperfusion injury, precisely to type 3 CRS. (AU)