Failure of acute hyperinsulinemia to alter blood pressure is not due to baroreceptor feedback

It is well documented that acute insulin administration stimulates the symp athetic nervous system in both humans and animals. Despite marked sympathet ic activation during acute hyperinsulinemia, blood pressure is generally no t increased because it is overridden by the vasodilator action of insulin. The maintenance of blood pressure in the face of sympathetic activation is unknown. A possible mechanism includes feedback regulation by the barorecep tor reflex are. Ln normotensive states, hyperinsulinemic-induced sympatheti c activation may tend to elevate blood pressure, but this change is rapidly sensed by the baroreceptors in the carotid arteries (and aortic arch), and a counterbalancing increase in vasodilation could return,blood pressure-to normal. Thus, it can be speculated that, in the event of diminished barore ceptor sensitivity and suppressed vasodilator actions of insulin, common ab normalities in hypertension, acute insulin infusion would be expected to in crease blood pressure. We undertook the present study to determine whether the baroreceptor reflex are modulated the blood pressure response to acute hyperinsulinemia. To th is end, six normotensive dogs underwent saline or insulin infusions before and after deactivation of the carotid and aortic baroreceptors. Barorecepto r dysfunction was documented after denervation in all cases by an abnormal response to phenylephrine injections. Before denervation, insulin infusions caused a slight but nonsignificant rise in mean arterial pressure (MAP; 11 0 +/- 5 to 120 +/- mm Hg; P = 0.13). Baroreceptor denervation caused a mark ed variability in blood pressure. However, basal mean arterial pressure was not significantly altered. Neither saline nor insulin infusions (105 +/- 1 0 v 105 +/- 8 mm Hg, basal v steady state) caused a significant change in M AP in denervated dogs. Likewise, insulin and saline did not change-heart-ra tes significantly in intact or denervated animals. Furthermore, glucose met abolism was similar in both groups of animals. This study demonstrates that the baroreceptor reflex are does not mediate the blood pressure response t o acute hyperinsulinemia. (C) 1999 American Journal of Hypertension, Ltd.