Human cardiac microvascular endothelial cells were treated with endothelin-1 in the presence of selective A<sub>2A</sub> or A<sub>2B</sub> agonists, or adenosine deaminase (ADA) inhibition, and profibrotic/oxidative stress genes were analyzed by qPCR.<h4>Results</h4>Hypertensive rats exhibited diastolic dysfunction with preserved systolic function, cardiac and renal fibrosis, oxidative/nitrative stress, and elevated pro-inflammatory cytokines. This evidence concerns the gene EDN1 and renal fibrosis.