Arterial baroreflex control of sympathetic nerve activity and heart rate in patients with type 2 diabetes.

Despite greater blood pressure reactivity to acute cardiovascular stressors and a higher prevalence of hypertension 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 yr; 31 ± 1 kg/m), 9 weight-matched controls (WM-CON, 46 ± 2 yr; 32 ± 2 kg/m) and 10 lean controls (Lean-CON, 49 ± 3 yr; 23 ± 1 kg/m), underwent bolus infusions of sodium nitroprusside (100 μg) followed 60 s later by phenylephrine (150 μg) and weighted linear regression performed. No group differences in overall sympathetic baroreflex gain were observed (T2D: -2.5 ± 0.3 vs. WM-CON: -2.6 ± 0.2 vs. Lean-CON: -2.7 ± 0.4 arbitrary units·beat·mmHg, P > 0.05) or in sympathetic baroreflex gain when derived separately during blood pressure (BP) falls (nitroprusside) and BP rises (phenylephrine). In contrast, overall cardiac baroreflex gain was reduced in T2D patients compared with Lean-CON (T2D: 8.2 ± 1.5 vs. Lean-CON: 15.6 ± 2.9 ms·mmHg, P < 0.05) and also tended to be reduced in WM-CON (9.3 ± 1.9 ms·mmHg) compared with Lean-CON (P = 0.059). Likewise, during BP rises, cardiac baroreflex gain was reduced in T2D patients and weight-matched controls compared with 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 with both obese and lean age-matched counterparts, with a selective impairment in ABR HR control in T2D that may be related to obesity.