Figure 4.

Insulin blunts catecholamine-induced vasoconstriction, in a β-adrenergic receptor-dependent manner, and augments β-adrenergic-mediated vasorelaxation. In protocol 3, mouse aortic rings were incubated with or without insulin for 30 min before stimulation with increasing concentrations of catecholamines (to assess vasoconstriction) or β-adrenergic receptor agonists (to assess vasorelaxation). A: insulin exposure blunts epinephrine- and norepinephrine-induced constriction in intact aortic rings. It also displays that this insulin-suppressing effect on catecholamine-induced constriction persists in aortic rings treated with nitric oxide synthase inhibitor l-NAME and in aortic rings devoid of the endothelium. Notably, such insulin-suppressing effect on catecholamine-induced constriction is diminished in rings treated with propranolol, a β-adrenergic receptor inhibitor. B: insulin exposure enhances isoproterenol (a nonspecific β-adrenergic receptor agonist)- and salbutamol (a β₂-adrenergic receptor agonist)-induced vasorelaxation in intact aortic rings. This insulin-potentiating effect on β-adrenergic-mediated vasorelaxation is largely lost in aortic rings treated with nitric oxide synthase inhibitor l-NAME and in aortic rings devoid of the endothelium. Data are reported as means ± SE (n = 8–10/condition). a.u., arbitrary units; AUC, area under the curve. Paired two-tailed Student’s t test (without insulin vs. with insulin) under each different experimental condition. *Significance (P < 0.05).