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Updated: Jul 2, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
Acute hyperglycemia and hyperinsulinemia enhance adrenergic vasoconstriction and decrease calcitonin gene-related
Yoshito Zamami1, Shingo Takatori, Kousuke Yamawaki
1Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Acute hyperglycemia and hyperinsulinemia worsen hypertension by increasing adrenergic nerve vasoconstriction and impairing calcitonin gene-related peptide nerve function. Insulin appears key in altering this neuronal vascular regulation.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Neuroscience
Background:
- Transient hyperglycemia and hyperinsulinemia are linked to hypertension development.
- Understanding their impact on vascular tone control is crucial.
Purpose of the Study:
- To investigate the effects of acute hyperglycemia and/or hyperinsulinemia on neuronal and humoral control of vascular tone in rats.
- To determine the specific roles of glucose and insulin in altering vascular responses.
Main Methods:
- Rats were anesthetized and pithed, with arterial blood pressure monitored.
- Vascular responses to spinal cord stimulation and vasoactive agents were assessed during glucose or insulin infusions.
- Specific interventions isolated the effects of hyperglycemia versus hyperinsulinemia.
Main Results:
- Glucose infusion (hyperglycemia and hyperinsulinemia) augmented adrenergic nerve-mediated pressor responses and attenuated calcitonin gene-related peptide (CGRP)-mediated depressor responses.
- Hyperglycemia alone (without hyperinsulinemia) primarily augmented adrenergic pressor responses.
- Hyperinsulinemia with euglycemia also augmented adrenergic pressor responses and attenuated CGRP depressor responses.
Conclusions:
- Acute hyperglycemia and hyperinsulinemia enhance adrenergic vasoconstriction and impair CGRP-mediated vasodilation.
- Increased plasma insulin concentration, associated with hyperglycemia, appears to be the primary driver of altered neuronal vascular regulation.
- These findings suggest a mechanism linking metabolic disturbances to hypertension via neurovascular dysfunction.
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