Role of the arterial baroreflex in the sympathetic response to hyperinsulinemia in adult humans

Abstract

Muscle sympathetic nerve activity (MSNA) increases during hyperinsulinemia, primarily attributed to central nervous system effects. Whether peripheral vasodilation induced by insulin further contributes to increased MSNA via arterial baroreflex-mediated mechanisms requires further investigation. Accordingly, we examined baroreflex modulation of the MSNA response to hyperinsulinemia. We hypothesized that rescuing peripheral resistance with co-infusion of the vasoconstrictor phenylephrine would attenuate the MSNA response to hyperinsulinemia. We further hypothesized the insulin-mediated increase in MSNA would be recapitulated with another vasodilator (sodium nitroprusside, SNP). Methods: In 33 young healthy adults (28M/5F), MSNA (microneurography) and arterial blood pressure (BP, Finometer/brachial catheter) were measured, and total peripheral resistance (TPR, ModelFlow) and baroreflex sensitivity were calculated at rest and during intravenous infusion of insulin (n=20) or SNP (n=13). A subset of participants receiving insulin (n=7) were co-infused with phenylephrine. Results: Insulin infusion decreased TPR (p=0.01) and increased MSNA (p<0.01), with no effect on arterial baroreflex sensitivity or BP (p>0.05). Co-infusion with phenylephrine returned TPR and MSNA to baseline, with no effect on arterial baroreflex sensitivity (p>0.05). Similar to insulin, SNP decreased TPR (p<0.05) and increased MSNA (p<0.01), with no effect on arterial baroreflex sensitivity (p>0.05). Conclusions: Acute hyperinsulinemia shifts the baroreflex stimulus-response curve to higher MSNA without changing sensitivity, likely due to insulin's peripheral vasodilatory effects. Results show peripheral vasodilation induced by insulin contributes to increased MSNA during hyperinsulinemia.

Altered Autonomic Function in Metabolic Syndrome: Interactive Effects of Multiple Components

“…Type 2 diabetes has been shown to significantly modulate muscle metaboreflexinduced peripheral vascular responses by way of enhancing muscle sympathetic nerve activity and the peripheral vasoconstrictor response similar to what is observed in hypertension [16,[95][96][97]. Furthermore, insulin itself, either in the context of diabetes development or via hyperinsulinemia, also exerts an effect on autonomic reflexes, such as the arterial baroreflex [98,99]. Pricher et al [100] reported that lateral ventricular insulin infusion in rats increased baroreflex control of both heart rate and lumbar sympathetic nerve activity.…”

Predictive Modeling of Resistant Hypertension Risk: Incorporating the TyG Index and Clinical Factors

“…IR primarily promotes sodium-potassium reabsorption in distal renal tubules by directly or indirectly increasing renin-angiotensin-aldosterone system activity, leading to increased reabsorption of sodium, potassium, and water in renal tubules and resulting in increased blood volume and cardiac output [24,25]. IR can also disrupt sympathetic nervous system function, increase peripheral and renal vascular resistance, impair endothelial function, cause lipid disorders and atherosclerosis; all of which are critical factors influencing RH [26,27]. Existing clinical studies have also found that IR is an independent risk factor for autonomic imbalance based on 6-month follow-up observations [28].…”

Differences in Heart Rate Variability and Baroreflex Sensitivity between Male and Female Athletes

“…Ensemble-R (Elucimed Ltd., Auckland, NZ, USA) provided systematic and monotonic three-beat increases or decreases in systolic BP and R-R intervals during controlled respiration [ 19 ]. The values were then paired as xy-coordinates to create a regression curve fitted to the BP and R-R signals [ 20 ]. We averaged slopes with correlation values of at least 0.8 for 300 s, which provided the upward sequences (BRS-up), downward sequences (BRS-down), and the average of the protocol (BRS-pooled) [ 21 ].…”