Letter to the editor: Sympathetically mediated increases in cardiac output, or peripheral vasoconstriction as primary regulator of BP during hyperinsulinemia?

摘要

to the editor: In the recent issue of the American Journal of Physiology-Heart and Circulatory Physiology, we read with interest the article by Limberg et al. (4) in which they attempt to discern the contributions of cardiac output (CO) and peripheral sympathetic vasoconstriction to the maintenance of arterial blood pressure (BP) during hyperinsulinemia in young healthy adults. We would like to applaud their translational approach, combining both in vivo and in vitro experiments to comprehensively investigate neural control of BP during hyperinsulinemia. The authors also used an innovative experimental design, applying 5-s pulses of neck suction (NS; —60 Torr) during basal and hyperinsulinemia conditions as a tool to examine the sympathetic restraint of leg blood flow. It was hypothesized that reducing sympathetic nerve activity (SNA) via NS during hyperinsulinemia would produce greater peripheral vasodilation and reduction in BP relative to NS under basal non-hyperinsulinemic conditions. The authors conclude that SNA-mediated increases in CO rather than peripheral vasoconstriction is the primary mechanism to maintain BP in the face of peripheral vasodilation caused by hyperinsulinemia. We would like to contribute to the discussion of these findings.