Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness

Yoshito Zamami, Shingo Takatori, Yukiko Iwatani, Kousuke Yamawaki, Satoko Miyashita, Nana Yabumae, Fusako Takayama, Mitsunobu Mio, Hiromu Kawasaki

Research output: Contribution to journalArticle

Abstract

Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated 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 generelated peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration 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 injection of pressor responses to 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 euglycemic, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases adrenergic nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.

Original languageEnglish
Pages (from-to)419-424
Number of pages6
JournalYakugaku Zasshi
Volume128
Issue number3
DOIs
Publication statusPublished - Mar 2008

Fingerprint

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

Keywords

  • Calcitonin gene-related peptide nerve
  • Hyperglycemia
  • Hyperinsulinemia

ASJC Scopus subject areas

  • Molecular Medicine

Cite this

Zamami, Y., Takatori, S., Iwatani, Y., Yamawaki, K., Miyashita, S., Yabumae, N., ... Kawasaki, H. (2008). Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness. Yakugaku Zasshi, 128(3), 419-424. https://doi.org/10.1248/yakushi.128.419

Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness. / Zamami, Yoshito; Takatori, Shingo; Iwatani, Yukiko; Yamawaki, Kousuke; Miyashita, Satoko; Yabumae, Nana; Takayama, Fusako; Mio, Mitsunobu; Kawasaki, Hiromu.

In: Yakugaku Zasshi, Vol. 128, No. 3, 03.2008, p. 419-424.

Research output: Contribution to journalArticle

Zamami, Y, Takatori, S, Iwatani, Y, Yamawaki, K, Miyashita, S, Yabumae, N, Takayama, F, Mio, M & Kawasaki, H 2008, 'Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness', Yakugaku Zasshi, vol. 128, no. 3, pp. 419-424. https://doi.org/10.1248/yakushi.128.419
Zamami Y, Takatori S, Iwatani Y, Yamawaki K, Miyashita S, Yabumae N et al. Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness. Yakugaku Zasshi. 2008 Mar;128(3):419-424. https://doi.org/10.1248/yakushi.128.419
Zamami, Yoshito ; Takatori, Shingo ; Iwatani, Yukiko ; Yamawaki, Kousuke ; Miyashita, Satoko ; Yabumae, Nana ; Takayama, Fusako ; Mio, Mitsunobu ; Kawasaki, Hiromu. / Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness. In: Yakugaku Zasshi. 2008 ; Vol. 128, No. 3. pp. 419-424.
@article{7370a4a2e9b5412e87b563e977673cf3,
title = "Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness",
abstract = "Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated 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 generelated peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration 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 injection of pressor responses to 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 euglycemic, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases adrenergic nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.",
keywords = "Calcitonin gene-related peptide nerve, Hyperglycemia, Hyperinsulinemia",
author = "Yoshito Zamami and Shingo Takatori and Yukiko Iwatani and Kousuke Yamawaki and Satoko Miyashita and Nana Yabumae and Fusako Takayama and Mitsunobu Mio and Hiromu Kawasaki",
year = "2008",
month = "3",
doi = "10.1248/yakushi.128.419",
language = "English",
volume = "128",
pages = "419--424",
journal = "Yakugaku Zasshi",
issn = "0031-6903",
publisher = "Pharmaceutical Society of Japan",
number = "3",

}

TY - JOUR

T1 - Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness

AU - Zamami, Yoshito

AU - Takatori, Shingo

AU - Iwatani, Yukiko

AU - Yamawaki, Kousuke

AU - Miyashita, Satoko

AU - Yabumae, Nana

AU - Takayama, Fusako

AU - Mio, Mitsunobu

AU - Kawasaki, Hiromu

PY - 2008/3

Y1 - 2008/3

N2 - Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated 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 generelated peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration 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 injection of pressor responses to 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 euglycemic, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases adrenergic nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.

AB - Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated 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 generelated peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration 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 injection of pressor responses to 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 euglycemic, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases adrenergic nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.

KW - Calcitonin gene-related peptide nerve

KW - Hyperglycemia

KW - Hyperinsulinemia

UR - http://www.scopus.com/inward/record.url?scp=40449103728&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=40449103728&partnerID=8YFLogxK

U2 - 10.1248/yakushi.128.419

DO - 10.1248/yakushi.128.419

M3 - Article

C2 - 18311062

AN - SCOPUS:40449103728

VL - 128

SP - 419

EP - 424

JO - Yakugaku Zasshi

JF - Yakugaku Zasshi

SN - 0031-6903

IS - 3

ER -