Abstract 018: Sympathetic Contribution to Obesity Hypertension: Differential Hemodynamic Mechanisms between Prehypertension and Hypertension
Sympathetic activation contributes to blood pressure (BP) elevation in obesity, but it is unknown whether this contribution differs between obese prehypertensives (PreHTN) and obese hypertensives (HTN). We, therefore, assessed hemodynamic parameters during autonomic withdrawal with the ganglionic blocker trimethaphan (TMT) in 15 lean normotensives (NTN; 34±3 yrs., BMI 23.4±0.4), 11 obese PreHTN (38±2 yrs., BMI 33.6±0.8) and 14 obese HTN (40±1 yrs., BMI 33.8±0.7). As expected, baseline supine systolic BP (SBP) was higher in PreHTN and HTN compared to NTN (P<0.01, Figure A). HTN, however, had lower supine SBP on the study day compared to their seated levels at screening (127±4 mmHg vs. 142±5; P=0.04) presumably due to lower sympathetic tone at supine rest. Autonomic blockade lowered SBP similarly in PreHTN (-23±4 mmHg) and HTN (-24±4 mmHg) compared to NTN (-8±3 mmHg; P<0.01), but the “intrinsic” SBP in the absence of autonomic influences remained slightly higher in HTN compared to the other groups. Baseline systemic vascular resistance (SVR) was similarly increased in PreHTN and HTN compared to NTN (P<0.01, Figure B), but it normalized after TMT only in PreHTN. Conversely, the BP drop in HTN was due to a decrease in cardiac output (CO; Figure C) and stroke volume (SV; -37±2 vs. PreHTN -25±2 and NTN -26±3%; P<0.01). In conclusion, the autonomic contribution to BP elevation differed between obese PreHTN and HTN. Obesity prehypertension was due to a sympathetically driven increase in SVR, whereas obesity hypertension was due to a non-autonomic increase in SVR associated with impaired sympathetic modulation of CO and SV presumably due to sympathetic contraction of splanchnic capacitance.
Author Disclosures: L.E. Okamoto: None. A. Gamboa: None. C. Shibao: None. A.C. Arnold: None. J.E. Celedonio: None. A. Diedrich: None. G. Farley: None. S.Y. Paranjape: None. I. Biaggioni: None.
- © 2014 by American Heart Association, Inc.