Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans.

Abstract

Euglycemic hyperinsulinemia evokes both sympathetic activation and vasodilation in skeletal muscle, but the mechanism remains unknown. To determine whether insulin per se or insulin-induced stimulation ofcarbohydrate metabolism is the main excitatory stimulus, we performed, in six healthy lean subjects, simultaneous microneurographic recordings of muscle sympathetic nerve activity, plethysmographic measurements of calf blood flow, and calorimetric determinations of carbohydrate oxidation rate. Measurements were made during 2 h of: (a) insulin/glucose infusion (hyperinsulinemic 16 pmol/kg per min] euglycemic clamp), (b) exogenous glucose infusion at a rate matched to that attained during protocol a, and (c) exogenous fructose infusion at the same rate as for glucose infusion in protocol b. For a comparable rise in carbohydrate oxidation, insulin/glucose infusion that resulted in twofold greater increases in plasma insulin concentrations than did glucose infusion alone, evoked twofold greater increases in both muscle sympathetic nerve activity and calf blood flow. Fructose infusion, which increased carbohydrate oxidation comparably, but had only a minor effect on insulinemia, did not stimulate either muscle sympathetic nerve activity or calf blood flow. These observations suggest that in humans hyperinsulinemia per se, rather than insulin-induced stimulation of carbohydrate metabolism, is the main mechanism that triggers both sympathetic activation and vasodilation in skeletal muscle. (J. Clin. Invest. 1993. 92:147-154.) Key words: energy expenditure * fructose infusion * glucose infusion * microneurography -hyperinsulinemic euglycemic clamp

Disparity of autonomic control in type 2 diabetes mellitus

“…Considering all these reports together with our findings, we suggest that sympathetic nerve hyperactivity in obese subjects could be explained by the presence of insulinaemia and insulin resistance. Our new findings are consistent with those in a large number of reports in experimental animals and normal humans showing that an increase in plasma insulin levels causes a nonuniform activation of the sympathetic drive [1][2][3][4][5][6][7][8][9][10][11][12]. For instance, in experimental animals, administration of insulin into the cerebral ventricles or intravenously has been shown to increase sympathetic nerve activity in efferent lumbar nerves without affecting efferent renal or adrenal nerves [6,7].…”

“…Extensive research shows that in normal healthy individuals acute hyperinsulinaemia in itself increases resting sympathetic output [1]. This has been shown using techniques such as venous plasma catecholamine concentration [2] and total body and forearm norepinephrine spillover [3] as well as by direct neural recordings [4,5].…”

Physiological hyperinsulinaemia increases intramuscular microvascular reactive hyperaemia and vasomotion in healthy volunteers

“…Evidently this and other possible mechanisms in intramuscular reactive hyperaemia, as well as the insulin-mediated effects on these mechanisms, need to be further investigated. In our study, as in many previous studies, insulin increased total leg blood flow [8,17,26]. This may have contributed to insulin-mediated changes in intramuscular reactive hyperaemia.…”

Suppression of Alcohol-Induced Hypertension by Dexamethasone

“…Data on heart rate (monitored with an electrocardiograph), respiratory excursions (pneumobelt), blood pressure (Finapres blood-pressure monitor [Ohmeda, Englewood, Colo.]), 20 blood flow in the calf (venous-occlusion plethysmography), 20 and sympathetic-nerve activity in efferent nerves were recorded continuously on an electrostatic recorder and a tape recorder (R71, TEAC, Tokyo, Japan). Respiratory excursions were monitored to detect the inadvertent performance of a Valsalva maneuver or prolonged expiration, since these respiratory maneuvers can stimulate sympathetic outflow.…”

“…Respiratory excursions were monitored to detect the inadvertent performance of a Valsalva maneuver or prolonged expiration, since these respiratory maneuvers can stimulate sympathetic outflow. 20 Intravenous catheters were inserted in a right and a left antecubital vein, one for the alcohol infusion and the other for blood sampling.…”