INSULIN REDUCES REFLEX FOREARM SYMPATHETIC VASOCONSTRICTION IN HEALTHY HUMANS

Previous in vitro studies indicate that insulin modifies vascular reac tivity to different agents. We have previously demonstrated that in no rmotensive humans physiological hyperinsulinemia is associated with an increase of forearm norepinephrine release but does not modify vascul ar resistance. To explore whether insulin modulates peripheral vasocon striction induced by reflex sympathetic activation, we studied its eff ects on forearm hemodynamics (strain-gauge plethysmography) during gra ded levels of lower body negative pressure (-5, -10, -15, and -20 mm H g, each for 5 minutes) in normotensive subjects. For this purpose, eig ht subjects received an intrabrachial artery infusion of regular insul in at a systemically ineffective rate (0.05 milliunits/kg per minute) so that deep-venous insulin levels increased in the experimental forea rm from 16.5+/-2.9 to 379.6+/-30 pmol/L (p<0.01), whereas arterial ins ulin levels remained unchanged (from 40.9+/-8.6 to 43.1+/-7.9 pmol/L, NS). In the control arm, forearm vascular resistance (units) increased from 52.3+/-3 to a peak of 78.4+/-5 (p<0.001) during lower body negat ive pressure. In the insulin-exposed forearm, vascular resistance (46. 4+/-2 at baseline) remained unchanged during insulin infusion (45.8+/- 3, NS) and rose to a peak of 54.8+/-6 (p<0.05) during lower body negat ive pressure. The response of forearm vascular resistance to lower bod y negative pressure was different in the two forearms (F=4.506, p<0.01 , repeated-measures analysis of variance with grouping factor). Our re sults demonstrate that in normotensive subjects local physiological hy perinsulinemia reduces the forearm vasoconstrictive response to reflex sympathetic activation.