title: Growth-dependent changes in the contribution of carbon monoxide to arteriolar function.
abstract: OBJECTIVE
  Endothelium-dependent dilation of skeletal muscle arterioles is mediated by unknown factors in very young rats. We assessed the possible contribution of carbon monoxide (CO) to this dilation and to dilation in older animals.
  
  
  METHODS
  The effects of de-endothelialization or various pharmacological inhibitors on responses to CO or endothelium-dependent dilators were studied in gracilis muscle arterioles from rats at 3-4 weeks ('weanlings') and 6-7 weeks ('juveniles').
  
  
  RESULTS
  Exogenous CO constricted, rather than dilated, arterioles from both age groups. This constriction was reduced by endothelial removal or NOS inhibition in juvenile, but not weanling, arterioles. In contrast, this constriction was abolished by K(+) channel inhibition in weanling, but not juvenile, arterioles. The heme precursor delta-aminolevulinic acid constricted juvenile arterioles but did not affect weanling arterioles. The heme oxygenase inhibitor chromium (III) mesoporphyrin IX abolished the endothelium-dependent dilation of juvenile arterioles to simvastatin, and reduced ACh- and simvastatin-induced dilations of weanling arterioles.
  
  
  CONCLUSIONS
  These findings suggest that relatively high concentrations of exogenous CO can cause constriction by inhibiting endothelium-derived NO in juvenile arterioles and inhibiting K(+) channels in weanling arterioles. Endogenous CO produced at lower concentrations can contribute to endothelium-dependent dilation in both age groups.
authors: Department of Physiology and Pharmacology, and Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, Morgantown, W. Va., USA.
authors: Julie Balch
authors: JB
authors: Samora
authors: Adam G
authors: AG
authors: Goodwill
authors: Jefferson C
authors: JC
authors: Frisbee
authors: Matthew A
authors: MA
authors: Boegehold
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000367:Age Factors; D000375:Aging; D000622:Aminolevulinic Acid / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism; D002245:Carbon Dioxide / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D006419:Heme Oxygenase (Decyclizing) / Q000037:antagonists & inhibitors / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008652:Mesoporphyrins / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000098:blood supply*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010455:Peptides / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D019821:Simvastatin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D004791:Enzyme Inhibitors; D008652:Mesoporphyrins; D010455:Peptides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C427471:chromium mesoporphyrin; D002245:Carbon Dioxide; D009569:Nitric Oxide; C064719:iberiotoxin; D000622:Aminolevulinic Acid; D019821:Simvastatin; D019001:Nitric Oxide Synthase; D006419:Heme Oxygenase (Decyclizing); D000109:Acetylcholine; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester