Role of the Autonomic Nervous System in the Hemodynamic Response to Hyperinsulinemia-Implications for Obesity and Insulin Resistance

Purpose of Review Herein, we summarize recent advances which provide new insights into the role of the autonomic nervous system in the control of blood flow and blood pressure during hyperinsulinemia. We also highlight remaining gaps in knowledge as it pertains to the translation of findings to relevant human chronic conditions such as obesity, insulin resistance, and type 2 diabetes. Recent Findings Our findings in insulin-sensitive adults show that increases in muscle sympathetic nerve activity with hyperinsulinemia do not result in greater sympathetically mediated vasoconstriction in the peripheral circulation. Both an attenuation of alpha-adrenergic-receptor vasoconstriction and augmented beta-adrenergic vasodilation in the setting of high insulin likely explain these findings. In the absence of an increase in sympathetically mediated restraint of peripheral vasodilation during hyperinsulinemia, blood pressure is supported by increases in cardiac output in insulin-sensitive individuals. We highlight a dynamic interplay between central and peripheral mechanisms during hyperinsulinemia to increase sympathetic nervous system activity and maintain blood pressure in insulin-sensitive adults. Whether these results translate to the insulin-resistant condition and implications for long-term cardiovascular regulation warrants further exploration.

Automated summary

This review summarizes recent advances in understanding the role of the autonomic nervous system in controlling blood flow and blood pressure during hyperinsulinemia. It emphasizes the need for further exploration on the translation of findings to chronic conditions such as obesity, insulin resistance, and type 2 diabetes. The findings suggest that, in insulin-sensitive adults, increased muscle sympathetic nerve activity during hyperinsulinemia does not lead to greater sympathetic vasoconstriction in the peripheral circulation. Instead, the attenuated alpha-adrenergic receptor constriction and enhanced beta-adrenergic vasodilation likely explain the observed results. The increase in blood pressure in insulin-sensitive individuals is primarily supported by an increase in cardiac output, as there is no increase in sympathetically mediated restraint of peripheral vasodilation during hyperinsulinemia. These findings highlight the complex interplay between central and peripheral mechanisms in regulating sympathetic nervous system activity and maintaining blood pressure during hyperinsulinemia. Further exploration is needed to determine if these results are applicable to insulin-resistant conditions and their long-term implications for cardiovascular regulation.