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 gene-related 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.
authors.affiliation: Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama City, Japan.
authors.forename: Yoshito
authors.initials: Y
authors.lastname: Zamami
authors.forename: Shingo
authors.initials: S
authors.lastname: Takatori
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Iwatani
authors.forename: Kousuke
authors.initials: K
authors.lastname: Yamawaki
authors.forename: Satoko
authors.initials: S
authors.lastname: Miyashita
authors.forename: Nana
authors.initials: N
authors.lastname: Yabumae
authors.forename: Fusako
authors.initials: F
authors.lastname: Takayama
authors.forename: Mitsunobu
authors.initials: M
authors.lastname: Mio
authors.forename: Hiromu
authors.initials: H
authors.lastname: Kawasaki
mesh_terms: D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000502:physiology; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology*; D006946:Hyperinsulinism / Q000503:physiopathology*; D008297:Male; D019518:Postprandial Period / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000502:physiology; D014661:Vasoconstriction
chemical_list: D015740:Calcitonin Gene-Related Peptide