The concomitant presence of obesity and hypertension was associated with significantly greater muscle sympathetic nerve activity (62.1 vs 32.2 bursts/100 beats, P<0.01) than either condition alone.
Observational (n=59)
Does the concomitant presence of obesity and hypertension synergistically increase sympathetic activity and impair baroreflex cardiovascular control compared to either condition alone?
The combination of obesity and hypertension triggers a greater sympathetic activation and impairment in baroreflex cardiovascular control than either condition alone.
Absolute Event Rate: 62.1% vs 32.2%
p-value: p=<0.01
Previous studies have shown that essential hypertension and obesity are both characterized by sympathetic activation coupled with a baroreflex impairment. The present study was aimed at determining the effects of the concomitant presence of the 2 above-mentioned conditions on sympathetic activity as well as on baroreflex cardiovascular control. In 14 normotensive lean subjects (aged 33. 5+/-2.2 years, body mass index 22.8+/-0.7 kg/m(2) mean+/-SEM), 16 normotensive obese subjects (body mass index 37.2+/-1.3 kg/m(2)), 13 lean hypertensive subjects (body mass index 24.0+/-0.8 kg/m(2)), and 16 obese hypertensive subjects (body mass index 37.5+/-1.3 kg/m(2)), all age-matched, we measured beat-to-beat arterial blood pressure (by Finapres device), heart rate (HR, by ECG), and postganglionic muscle sympathetic nerve activity (MSNA, by microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Blood pressure values were higher in lean hypertensive and obese hypertensive subjects than in normotensive lean and obese subjects. MSNA was significantly (P:<0.01) greater in obese normotensive subjects (49.1+/-3.0 bursts per 100 heart beats) and in lean hypertensive subjects (44.5+/-3.3 bursts per 100 heart beats) than in lean normotensive control subjects (32.2+/-2.5 bursts per 100 heart beats); a further increase was detectable in individuals with the concomitant presence of obesity and hypertension (62.1+/-3. 4 bursts per 100 heart beats). Furthermore, whereas in lean hypertensive subjects, only baroreflex control of HR was impaired, in obese normotensive subjects, both HR and MSNA baroreflex changes were attenuated, with a further attenuation being observed in obese hypertensive patients. Thus, the association between obesity and hypertension triggers a sympathetic activation and an impairment in baroreflex cardiovascular control that are greater in magnitude than those found in either of the above-mentioned abnormal conditions alone.
Grassı et al. (Sun,) conducted a observational in Obesity and hypertension (n=59). Concomitant obesity and hypertension vs. Lean normotensive subjects was evaluated on Postganglionic muscle sympathetic nerve activity (MSNA) at rest (bursts per 100 heart beats) (p=<0.01). The concomitant presence of obesity and hypertension was associated with significantly greater muscle sympathetic nerve activity (62.1 vs 32.2 bursts/100 beats, P<0.01) than either condition alone.