Does acute hyperinsulinemia induce selective hemodynamic effects and does nitric oxide play a role in regulating blood flow and MAP in anesthetized dogs?
Acute hyperinsulinemia redistributes blood supply to preserve skeletal muscle irrigation while reducing renal blood flow, a process mediated by nitric oxide.
The purpose of this study was to investigate whether acute hyperinsulinemia induces selective hemodynamic effects in the mesenteric, renal, and iliac vascular beds, and to determine whether nitric oxide (NO) plays a role in the regulation of blood flow and mean arterial pressure (MAP) during acute hyperinsulinism. In eight anesthetized dogs (Group A), the response to a hyperinsulinemic test was determined before and after NO inhibition, with L-nitro-arginine methyl esther (L-NAME), during the last 45 min of the experiment. In seven dogs (Group B), NO inhibition was induced before and maintained throughout hyperinsulinemia. In Group A, the hyperinsulinemic test did not alter MAP, but induced a significant reduction in both renal and mesenteric blood flow without a significant change in iliac blood flow. In contrast, the administration of L-NAME in Group B was followed by a significant decrease in mesenteric, renal, and iliac blood flow, but mean arterial pressure remained unchanged. In this group, hyperinsulinemia instituted after the blockade of NO was followed by a significant elevation in blood pressure levels, concomitant with reductions in blood flow to the three vascular beds. In summary, acute hyperinsulinemia induced a redistribution of blood supply, which preserves skeletal muscle irrigation while reducing blood flow to the kidney. Nitric oxide participates in this redistribution because L-NAME infusion abolishes the compensatory influence on skeletal muscle blood flow.
Villa et al. (Thu,) studied this question.