André J Scheen1,2. 1. Division of Diabetes, Nutrition and Metabolic Disorders, Department of Medicine, CHU Liège, University of Liège, CHU Sart Tilman (B35), 4000, Liège, Belgium. andre.scheen@chu.ulg.ac.be. 2. Clinical Pharmacology Unit, CHU Liège, Center for Interdisciplinary Research on Medicines (CIRM), University of Liège, Liège, Belgium. andre.scheen@chu.ulg.ac.be.
Abstract
PURPOSE OF THE REVIEW: Hyperactivity of sympathetic nervous system (SNS) plays a role in the development of arterial hypertension and heart failure, two co-morbidities frequently associated with type 2 diabetes (T2DM). This review aims at analyzing the effects of sodium-glucose cotransporter type 2 inhibitors (SGLT2is) on blood pressure and more especially on SNS activity in patients with T2DM. RECENT FINDINGS: By enhancing glucosuria, natriuresis, and osmotic diuresis, SGLT2is improve glucose control, promote weight loss, lower arterial blood pressure, and reduce the risk of major cardiovascular events and hospitalization for heart failure. No rise of heart rate is detected despite reductions in blood pressure and plasma volume, which may suggest a dampening of SNS activity. Indeed, increasing experimental and clinical data demonstrated a reduction in SNS activity, including in key target organs such as the heart and the kidneys. Of potential major interest, a better understanding of the mechanisms linking SGLT2 and SNS deserves further investigation.
PURPOSE OF THE REVIEW: Hyperactivity of sympathetic nervous system (SNS) plays a role in the development of arterial hypertension and heart failure, two co-morbidities frequently associated with type 2 diabetes (T2DM). This review aims at analyzing the effects of sodium-glucose cotransporter type 2 inhibitors (SGLT2is) on blood pressure and more especially on SNS activity in patients with T2DM. RECENT FINDINGS: By enhancing glucosuria, natriuresis, and osmotic diuresis, SGLT2is improve glucose control, promote weight loss, lower arterial blood pressure, and reduce the risk of major cardiovascular events and hospitalization for heart failure. No rise of heart rate is detected despite reductions in blood pressure and plasma volume, which may suggest a dampening of SNS activity. Indeed, increasing experimental and clinical data demonstrated a reduction in SNS activity, including in key target organs such as the heart and the kidneys. Of potential major interest, a better understanding of the mechanisms linking SGLT2 and SNS deserves further investigation.
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