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Decreased microvascular vasomotion and myogenic response in rat skeletal muscle in association with acute insulin resistance
journal contributionposted on 2023-05-17, 00:40 authored by Newman, JMB, Renee RossRenee Ross, St Pierre, P, Stephen RichardsStephen Richards, Michael ClarkMichael Clark, Stephen RattiganStephen Rattigan
In addition to increased glucose uptake, insulin action is associated with increased total and microvascular blood flow, and vasomotion in skeletal muscle. The aim of this study was to determine the effect of acute insulin resistance caused by the peripheral vasoconstrictor á-methylserotonin (áMT) on microvascular vasomotion in muscle. Heart rate (HR), mean arterial pressure (MAP), femoral blood flow (FBF), whole body glucose infusion (GIR) and hindleg glucose uptake (HGU) were determined during control and hyperinsulinaemic euglycaemic clamp conditions in anaesthetized rats receiving áMT infusion. Changes inmuscle microvascular perfusion were measured by laserDoppler flowmetry (LDF) and vasomotion was assessed by applying wavelet analysis to the LDF signal. Insulin increased GIR and HGU. Five frequency bands corresponding to cardiac, respiratory, myogenic, neurogenic and endothelial activities were detected in the LDF signal. Insulin infusion alone increased FBF (1.18±0.10 to 1.78±0.12 ml min–1, P<0.05), LDF signal strength (by 16% compared to baseline) and the relative amplitude of the myogenic component of vasomotion (0.89±0.09 to 1.18±0.06, P<0.05).When infused aloneáMTdecreased LDFsignal strength and themyogenic component of vasomotion by 23% and 27% respectively compared to baseline, but did not affect HGU or FBF. Infusion of áMT during the insulin clamp decreased the stimulatory effects of insulin on GIR, HGU, FBF and LDF signal and blocked the myogenic component of vasomotion. These data suggest that insulin action to recruit microvascular flow may in part involve action on the vascular smoothmuscle to increase vasomotion in skeletalmuscle to thereby enhance perfusion and glucose uptake. These processes are impaired with this model of áMT-induced acute insulin resistance.
Publication titleJournal of Physiology
Department/SchoolMenzies Institute for Medical Research
PublisherCambridge Univ Press
Place of publication40 West 20Th St, New York, USA, Ny, 10011-4211