Sympathetic Activity Increases With Obesity in Hypertensive Patients

Introduction: Obesity is one of the most important risk factors for the development of hypertension; the mechanisms by which obesity raises BP are not fully understood. Obesity leads to ↑ sympathetic autonomic nervous system (SANS) activity by several mediators such as leptin, ↓ nitric oxide, ↑ angiotensin II, ↓adiponectin, ↓ ghrelin and baroreflex dysfunction. Unknown is the role of dopamine, catecholamines and metanephrines in hypertensive individuals with obesity indexed by body mass index (BMI). Methods: In this prospective evaluation, 195 hypertensive patients on medications were recruited after ≥3 clinic visits at University of Alabama at Birmingham Hypertension Clinic. All patients underwent measurement of clinic BP, BMI and 24-hr urine for dopamine, total catecholamines (epinephrine and norepinephrine) and total metanephrines (metanephrine and normetanephrine). WHO obesity classification was used to categorize patients based on BMI into normal weight (BMI 18.5 to 24.9, n=19); over-weight (BMI 25 to 29.9, n=45); Class 1 obesity (BMI 30 to 34.9, n=46); Class 2 obesity (BMI 35 to 39.9, n=44) and Class 3 obesity (BMI greater than 40, n=36). Results: Overall, patients were 50% females, 56.8% African Americans, 58.1 ± 11.0 years old, BMI was 34.1 ± 7.1 Kg/m 2 , BP was 126.5/79.9 ± 20.2/12.3 mmHg and heart rate of 73.5 ± 12.5 beats/min and total number of BP medications were 3.8 ± 1.4. 24-hr urinary dopamine, norepinephrine, total catecholamines, normetanephrine and total metanephrines increased with increasing BMI categories. Conclusions: Increase in BMI is associated with increasing dopamine, catecholamines and metanephrines indicative of progressive SANS activation.