2008
DOI: 10.1291/hypres.31.1033
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Acute Hyperglycemia and Hyperinsulinemia Enhance Adrenergic Vasoconstriction and Decrease Calcitonin Gene-Related Peptide-Containing Nerve-Mediated Vasodilation in Pithed Rats

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Cited by 35 publications
(19 citation statements)
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“…45 Studies on glucose effects on neuropeptides are limited thus far, but there are indications that either dextrose elevations or a related reduction in insulin levels downregulate the activity of the transient receptor potential vanilloid type 1 (TRPV1) receptor which reduces production of pain producing (substance P) and degenerative (calcitonin gene-related peptide [CGRP]) neuropeptides. [46][47][48] …”
Section: Consideration Of Possible Mechanisms and Explanationsmentioning
confidence: 99%
“…45 Studies on glucose effects on neuropeptides are limited thus far, but there are indications that either dextrose elevations or a related reduction in insulin levels downregulate the activity of the transient receptor potential vanilloid type 1 (TRPV1) receptor which reduces production of pain producing (substance P) and degenerative (calcitonin gene-related peptide [CGRP]) neuropeptides. [46][47][48] …”
Section: Consideration Of Possible Mechanisms and Explanationsmentioning
confidence: 99%
“…Therefore, both adrenergic and CGRPergic nerves regulate the tone of resistance arteries by reciprocal interaction (Kawasaki et al, 1988(Kawasaki et al, , 1990. Previous reports demonstrated that an acute (insulin infusion) or chronic hyperinsulinemic state (FDR) caused increased adrenergic nerve-mediated vasoconstriction and decreased CGRPergic nervemediated vasodilatation, suggesting that hyperinsulinemia in FDR results in dysfunction of the neuronal vascular control system, leading to the development of hypertension (Takatori et al, 2006;Zamami et al, 2008). Therefore, the previous findings are supported by the present immunohistochemistry findings that hyperinsulinemia caused abnormal perivascular innervation in mesenteric resistance arteries of FDR resulting in increased adrenergic (TH-LI) nerve density and decreased CGRPergic (CGRP-LI) nerve density.…”
Section: Discussionmentioning
confidence: 99%
“…Taking all together, considering the observed reduction of the ischemic threshold (time to 1 mm ST-segment depression) associated to an increment of the ischemic burden (greater WMSI at stress echocardiography), it is likely that the mechanism by which HCM induced a greater ischemic impairment could be mainly related to an increase of vascular tone, confirming that acute hyperglycemia and hyperinsulinemia may increase adrenergic nerve-mediated vasoconstriction [29] and, consequentely, reduced coronary supply.…”
Section: Mechanisms Of Reduced Ischemic Threshold After Hcmmentioning
confidence: 92%