Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans
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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.Abstract:
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 microU/ml during control, to 72 +/- 8 and 144 +/- 13 microU/ml during the low and high insulin doses, respectively, and fell to 15 +/- 6 microU/ml 1 h after insulin infusion was stopped MSNA, which averaged 215 +/- 15 bursts/min in control, increased significantly (P less than 0001) during both the low and high doses of insulin (+/- 54 and +/- 93 bursts/min, respectively) and further increased during 1-h recovery (+152 bursts/min) Plasma norepinephrine levels (119 +/- 19 pg/ml during control) rose during both low (258 +/- 25; P less than 002) and high (285 +/- 95; P less than 001) doses of insulin and recovery (316 +/- 23; P less than 001) Plasma epinephrine levels did not change during insulin infusion Despite the increased MSNA and plasma norepinephrine, there were significant (P less than 0001) 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 approximately 4-5 mmHg (P less than 001) 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 humansread more
Citations
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References
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Role of Insulin Resistance in Human Disease
TL;DR: The possibility is raised that resistance to insulin-stimulated glucose uptake and hyperinsulinemia are involved in the etiology and clinical course of three major related diseases— NIDDM, hypertension, and CAD.
Journal ArticleDOI
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TL;DR: Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique] are described.
Journal ArticleDOI
Immunoassay of Endogenous Plasma Insulin in Man
TL;DR: For years investigators have sought an assay for insulin which would combine virtually absolute specificity with a high degree of sensitivity, sufficiently exquisite for measurement of the minute insulin concentrations usually present in the circulation as mentioned in this paper.
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Hyperinsulinemia. A link between hypertension obesity and glucose intolerance.
TL;DR: It is concluded that insulin resistance and/or hyperinsulinemia are present in the majority of hypertensives, constitute a common pathophysiologic feature of obesity, glucose intolerance, and hypertension, possibly explaining their ubiquitous association, and may be linked to the increased peripheral vascular resistance of hypertension, which is putatively related to elevated intracellular sodium concentration.
Journal ArticleDOI
Immunoassay of endogenous plasma insulin in man
TL;DR: The insulin concentration in plasma has been estimated from the degree of hypoglycemia produced in hypophysectomized, adrenalectomization, alloxan-diabetic rats, and from the increased oxidation of glucose-1-C14 by the rat epididymal fat pad.