Cardiovascular responses to insulin in the absence of hypoglycemia

Pereda, Santiago A.; Eckstein, John W.; Abboud, François M.

doi:10.1152/ajplegacy.1962.202.2.249

Cited by 75 publications

(45 citation statements)

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“…In this regard, an earlier study found a small but significant decrease in diastolic blood pressure during insulin/glucose infusion in humans (6). Alternatively, a central neural action of insulin may also contribute to stimulation of sympathetic outflow in this setting (8,(40)(41)(42)(43).…”

Section: Discussionmentioning

confidence: 94%

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

Vollenweider¹,

Tappy²,

Randin³

et al. 1993

J. Clin. Invest.

306

209

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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

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Section: Discussionmentioning

confidence: 94%

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

Vollenweider¹,

Tappy²,

Randin³

et al. 1993

J. Clin. Invest.

306

209

View full text Add to dashboard Cite

show abstract

“…Insulin-specific binding sites have been located in the hypothalamus of the rat brain (25), and intraventricular injections of insulin have been shown to increase CNS catecholamine turn-2250 over (26). Pereda et al (27) have shown that infusing insulin into the carotid arteries of dogs, at doses which have no effect when administered systematically, elevate arterial pressure.…”

Section: Discussionmentioning

confidence: 99%

Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.

Anderson¹,

Hoffman²,

Balon³

et al. 1991

J. Clin. Invest.

1,034

608

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Hyperinsulinemia may contribute to hypertension by increasing sympathetic activity and vascular resistance. We sought to determine if insulin increases central sympathetic neural outflow and vascular resistance in humans. We recorded muscle sympathetic nerve activity (MSNA; microneurography, peroneal nerve), forearm blood flow (plethysmography), heart rate, and blood pressure in 14 normotensive males during 1-h infusions of low (38 mU/m2/min) and high (76 mU/m2/min) doses of insulin while holding blood glucose constant. Plasma insulin rose from 8±1 uU/ml during control, to 72±8 and 144±13 MtU/ml during the low and high insulin doses, respectively, and fell to 15±6 gU/ml 1 h after insulin infusion was stopped.MSNA, which averaged 21.5±1.5 bursts/min in control, increased significantly (P < 0.001) during both the low and high doses of insulin (±5.4 and ±9.3 bursts/min, respectively) and further increased during 1-h recovery (+15.2 bursts/min). Plasma norepinephrine levels (119±19 pg/ml during control) rose during both low (258±25; P < 0.02) and high (285±95; P < 0.01) doses of insulin and recovery (316±23; P < 0.01). Plasma epinephrine levels did not change during insulin infusion. Despite the increased MSNA and plasma norepinephrine, there were significant (P < 0.001) increases in forearm blood flow and decreases in forearm vascular resistance during both doses of insulin. Systolic pressure did not change significantly during infusion of insulin and diastolic pressure fell -4-5 mmHg (P < 0.01). This study suggests that acute increases in plasma insulin within the physiological range elevate sympathetic neural outflow but produce forearm vasodilation and do not elevate arterial pressure in normal humans. (J. Clin. Invest.

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“…In an early study, a low dose of insulin injected into the carotid arteries of dogs increased blood pressure before a fall in blood glucose (27). A relationship between insulin sensitive regions in the hypothalamus and sympathetic activity was later established in experiments using gold thioglucose in mice (28).…”

Section: Direct Neural Mechanismsmentioning

confidence: 99%