RESUMO
Diabetes mellitus is a chronic metabolic disease, in which the abnormality of glucose and lipid metabolism may cause multisystem damage. Sodium-glucose synergistic transporter 2 (SGLT2) inhibitors are a novel type of hypoglycemic drug that can lower blood sugar level by inhibiting the absorption of glucose through renal tubules. Studies have shown that SGLT2 inhibitors also have a lowering effect on blood pressure, but the mechanism is not fully elucidated. In this article the hypotensive effects of SGLT2 inhibitors and possible mechanisms are reviewed.
RESUMO
The potential mechanism by which sodium-glucose cotransporter 2 (SGLT2) inhibitors prevent cardiovascular disease (CVD) is being widely investigated. Improved insulin resistance, along with decreased body fat mass associated with SGLT2 inhibitor treatment is consistent with previously well-established factors contributing to the prevention of CVD. These factors are responsible for reduction of oxidative stress as well as improvement of systemic inflammation. Because heart failure was one of the most dramatically improved cardiovascular events in various clinical trials and because SGLT2 inhibitors promote osmotic diuresis and natriuresis, hemodynamic changes are considered as a critical mechanism responsible for the cardioprotective effect of SGLT2 inhibitors. Restored tubuloglomerular feedback by SGLT2 inhibitors might play a role in renoprotection, which in turn, leads to fewer CVDs. Finally, blood ketone body increments in response to SGLT2 inhibition might act as a “super-fuel” for salvaging the failing diabetic heart.