Despite greater blood pressure reactivity to acute cardiovascular stressors in type 2 diabetes (T2D) patients, limited information is available regarding arterial baroreflex (ABR) control in T2D. We hypothesized that ABR control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) are attenuated in T2D patients. Seventeen T2D-patients (50±2 yrs; 31±1 kg/m2), 9 weight-matched controls (WM-CON, 46±2 yrs; 32±2 kg/m2) and 10 lean controls (Lean-CON, 49±3 yrs; 23±1 kg/m2), underwent bolus infusions of sodium nitroprusside (100μg) followed 60s later by phenylephrine (150μg) and weighted linear regression performed. No group differences in overall sympathetic baroreflex gain were observed (T2D-patients: -2.5±0.3 vs. WM-CON: -2.6±0.2 vs. Lean-CON: -2.7±0.4 AU·beat·mmHg-1, P>0.05) or in sympathetic baroreflex gain when derived separately during BP falls (nitroprusside) and BP rises (phenylephrine). In contrast, overall cardiac baroreflex gain was reduced in T2D-patients compared to Lean-CON (T2D-patients: 8.2±1.5 vs. Lean-CON: 15.6±2.9 ms·mmHg-1, P<0.05), and also tended to be reduced in WM-CON (9.3±1.9 ms·mmHg-1) compared to Lean-CON (P=0.059). Likewise, during BP rises, cardiac baroreflex gain was reduced in T2D-patients and weight-matched controls compared to lean controls (P<0.05), whereas no group differences were found during BP falls (P>0.05). Sympathetic and cardiac ABR gains were comparable between normotensive and hypertensive T2D-patients (P>0.05). These findings suggest preserved ABR control of MSNA in T2D-patients compared to both obese and lean age-matched counterparts, with a selective impairment in ABR HR control in T2D that may be related to obesity.
- muscle sympathetic nerve activity
- arterial blood pressure
- insulin resistance
- modified Oxford
- Copyright © 2016, American Journal of Physiology-Heart and Circulatory Physiology