Why the study?
The role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure was unclear.
Does sympathetic activation during hyperinsulinemia maintain blood pressure via increased cardiac output or restraint of peripheral vasodilation in healthy adults?
Does sympathetic activation during hyperinsulinemia maintain blood pressure via increased cardiac output or restraint of peripheral vasodilation in healthy adults?
Blood pressure maintenance during hyperinsulinemia is primarily driven by sympathetically mediated increases in cardiac output rather than peripheral vasoconstriction.
Refines hyperinsulinemia hemodynamics model; hypothesis-generating pending replication in cardiometabolic disease.
We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.
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Limberg et al. (2020) studied this question.
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