Acute hyperglycemia and hyperinsulinemia enhance adrenergic vasoconstriction and decrease calcitonin gene-related peptide-containing nerve-mediated vasodilation in pithed rats

Yoshito Zamami, Shingo Takatori, Kousuke Yamawaki, Satoko Miyashita, Mitsunobu Mio, Yoshihisa Kitamura, Hiromu Kawasaki

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Recent clinical studies have demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated the influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin gene-related peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentrations of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented adrenergic nerve-mediated pressor responses to SCS without affecting pressor responses to injection of noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of adrenergic nerve-mediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemia, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increase adrenergic nerve-mediated vasoconstriction, which in turn blunts CGRPergic nerve function, and that the increase in plasma insulin concentration associated with hyperglycemia may be responsible for the alteration of neuronal vascular regulation.

Original languageEnglish
Pages (from-to)1033-1044
Number of pages12
JournalHypertension Research
Volume31
Issue number5
DOIs
Publication statusPublished - May 2008

Fingerprint

Calcitonin Gene-Related Peptide
Hyperinsulinism
Vasoconstriction
Vasodilation
Hyperglycemia
Adrenergic Agents
Insulin
Spinal Cord Stimulation
Glucose
Blood Vessels
Nitroprusside
Angiotensin II
Acetylcholine
Blood Glucose
Norepinephrine
Serum
Injections
Octreotide
Intravenous Injections
Wistar Rats

Keywords

  • Adrenergic nerve-mediated pressor
  • Calcitonin gene-related peptide-containing nerve-mediated depressor
  • Hyperglycemia
  • Hyperinsulinemia
  • Spinal cord stimulation

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Acute hyperglycemia and hyperinsulinemia enhance adrenergic vasoconstriction and decrease calcitonin gene-related peptide-containing nerve-mediated vasodilation in pithed rats. / Zamami, Yoshito; Takatori, Shingo; Yamawaki, Kousuke; Miyashita, Satoko; Mio, Mitsunobu; Kitamura, Yoshihisa; Kawasaki, Hiromu.

In: Hypertension Research, Vol. 31, No. 5, 05.2008, p. 1033-1044.

Research output: Contribution to journalArticle

Zamami, Yoshito ; Takatori, Shingo ; Yamawaki, Kousuke ; Miyashita, Satoko ; Mio, Mitsunobu ; Kitamura, Yoshihisa ; Kawasaki, Hiromu. / Acute hyperglycemia and hyperinsulinemia enhance adrenergic vasoconstriction and decrease calcitonin gene-related peptide-containing nerve-mediated vasodilation in pithed rats. In: Hypertension Research. 2008 ; Vol. 31, No. 5. pp. 1033-1044.
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AU - Takatori, Shingo

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AB - Recent clinical studies have demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated the influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin gene-related peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentrations of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented adrenergic nerve-mediated pressor responses to SCS without affecting pressor responses to injection of noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of adrenergic nerve-mediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemia, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increase adrenergic nerve-mediated vasoconstriction, which in turn blunts CGRPergic nerve function, and that the increase in plasma insulin concentration associated with hyperglycemia may be responsible for the alteration of neuronal vascular regulation.

KW - Adrenergic nerve-mediated pressor

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KW - Hyperinsulinemia

KW - Spinal cord stimulation

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