title: Human skeletal muscle feed arteries studied in vitro: the effect of temperature on α(1)-adrenergic responsiveness.
abstract: Heat and cold exposure can decrease and increase total peripheral resistance, respectively, in humans. With unique access to human skeletal muscle feed arteries, we sought both to characterize these vessels and to determine the interaction between temperature and α(1)-adrenergic receptor responsiveness. We hypothesized that α(1)-mediated vasocontraction of human feed arteries would be attenuated in response to 39 or 35°C. Skeletal muscle feed arteries were harvested from thirty-two human volunteers and studied using isometric techniques. Vessel function was assessed using KCl, sodium nitroprusside (SNP), phenylephrine (PE) and ACh dose-response curves to characterize non-receptor- and receptor-mediated vasocontraction and vasorelaxation. Single doses of PE (1 mm) and KCl (100 mm) were administered at 37°C and then, in a balanced design, repeated at both 35 and 39°C. The KCl and PE dose-response curves elicited significant vasocontraction (2009 ± 407 and 1974 ± 508 mg developed tension, respectively), whereas SNP and ACh induced the expected vasorelaxation (102 ± 6 and 73 ± 10% relaxation, respectively). Altering the temperature had no effect on inherent smooth muscle function (KCl response), but both a reduction (35°C) and an increase in temperature (39°C) decreased the vasocontractile response to 1 mm PE (37°C, 1478 ± 338 mg; 35°C, 546 ± 104 mg; and 39°C, 896 ± 202 mg; P < 0.05) or across PE dose (P < 0.05, 35 and 39 versus 37°C). Despite clear heterogeneity between both the human volunteers and the feed arteries themselves, this novel approach to the procurement of human vessels revealed a robust 'inverted U' response to altered temperature, such that α(1)-mediated vasocontraction was attenuated with either warming or cooling.
authors.affiliation: Geriatric Research Education and Clinical Center, George E. Whalen VA Medical Center, Salt Lake City, UT, USA.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Ives
authors.forename: Robert H I
authors.initials: RH
authors.lastname: Andtbacka
authors.forename: R Dirk
authors.initials: RD
authors.lastname: Noyes
authors.forename: John
authors.initials: J
authors.lastname: McDaniel
authors.forename: Markus
authors.initials: M
authors.lastname: Amann
authors.forename: Melissa A H
authors.initials: MA
authors.lastname: Witman
authors.forename: J David
authors.initials: JD
authors.lastname: Symons
authors.forename: D Walter
authors.initials: DW
authors.lastname: Wray
authors.forename: Russell S
authors.initials: RS
authors.lastname: Richardson
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001158:Arteries / Q000502:physiology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply*; D009599:Nitroprusside; D009638:Norepinephrine; D010656:Phenylephrine; D011189:Potassium Chloride; D018340:Receptors, Adrenergic, alpha-1 / Q000187:drug effects / Q000502:physiology*; D013696:Temperature; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000316:Adrenergic alpha-Agonists; D018340:Receptors, Adrenergic, alpha-1; D009599:Nitroprusside; D010656:Phenylephrine; D011189:Potassium Chloride; D009638:Norepinephrine