title: Glycemic modulation of insulin/IGF-1 mediated skeletal muscle blood following sympathetic denervation in normal rats.
abstract: Both insulin and IGF-1 decrease vascular resistance and increase blood flow in skeletal muscle, and it has been suggested that the mechanistic action for insulin may be by increasing autonomic vasodilatory activity. In this study we evaluated the effects of insulin and IGF-1 on blood flow to denervated and non-denervated skeletal muscle as part of a continuing investigation into the mechanism of regulation of cardiovascular responses by these hormones. Normal rats were prepared for measurements of mean arterial pressure (MAP), heart rate (HR) and vascular flow in the left and right iliac artery. Resection of the left lumbar sympathetic chain increased flow (expressed as conductance, flow/MAP) in the denervated left iliac but not in the intact right artery. Subsequent insulin infusion where hypoglycemia was allowed to occur increased conductance in both arteries, but more so in the denervated artery. Similarly, IGF-1 infusion increased conductances in both intact and denervated iliac arteries, and the effect was slightly greater in the denervated artery. Insulin infusion when euglycemia was maintained increased conductance to a similar extent in denervated and intact iliac arteries. Contrastingly, IGF-1 infusion under euglycemic conditions resulted in a much greater increased conductance in the intact iliac. We conclude that both insulin and IGF-1 increase conductance directly and that glycemic status and sympathetic nerve activity modulate these responses. The insulin-induced increase in conductance in the denervated limb under hypoglycemic conditions suggest that hypoglycemic-stimulated epinephrine release may enhance the dilatory response. while the greater response to IGF-1 in the intact vessel under euglycemic conditions may be due to IGF-1 capacity to decrease sympathetic activity leading to an enhanced conductance.
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Duanmu
authors.forename: T
authors.initials: T
authors.lastname: Scislo
authors.forename: J C
authors.initials: JC
authors.lastname: Dunbar
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D006339:Heart Rate / Q000187:drug effects; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007083:Iliac Artery / Q000502:physiology; D007328:Insulin / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D008160:Lumbosacral Plexus / Q000601:surgery; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000502:physiology
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D007334:Insulin-Like Growth Factor I; D005947:Glucose