Diabetes is among the leading causes of morbidity and mortality worldwide. New antidiabetics - gliflozins (inhibitors of sodium-glucose transporter 2) show many beneficial actions beyond their hypoglycemic effects. The underlying mechanisms of these additional cardiorenal protective effects are still not well understood, especially in hypertensive non-diabetic disease. The pathophysiology of three hypertensive rat strains (hereditary hypertriglyceridemic rats, spontaneously hypertensive rats with human CRP transgene and heterozygous Ren-2 transgenic rats) is completely different. Thus, the evaluation of metabolic changes, the changes of gene expression profiles and the role of inflammation in organ damage following chronic empagliflozin treatment in advanced stages of the disease could be valuable for detailed understanding of the mechanisms of gliflozins beneficial effects.