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Am J Physiol Heart Circ Physiol 284: H1073-H1079, 2003; doi:10.1152/ajpheart.00881.2002
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Vol. 284, Issue 4, H1073-H1079, April 2003

Carbon monoxide mediates vasodilator effects of glutamate in isolated pressurized cerebral arterioles of newborn pigs

Elisa Fiumana, Helena Parfenova, Jonathan H. Jaggar, and Charles W. Leffler

Laboratory for Research in Neonatal Physiology, Departments of Physiology and Pediatrics, Vascular Biology Center, University of Tennessee Health Science Center, Memphis, Tennessee 38163

The excitatory neurotransmitter glutamate causes dilation of newborn pig cerebral arterioles in vivo that is blocked by inhibition of carbon monoxide (CO) production. CO, a potent dilator in cerebral circulation in vivo, is produced endogenously in cerebral microvessels via heme oxygenase (HO). In isolated pressurized cerebral arterioles (~200 µm) from newborn pigs, we investigated the involvement of CO and the endothelium in response to glutamate. A CO-releasing molecule, dimanganese decacarbonyl (10-8-10-6 M), dilated cerebral arterioles. Glutamate (10-6-10-4 M) and 1-aminocyclopentane-cis-1,3-dicarboxylic acid (cis-ACPD; 10-6-10-5 M), a N-methyl-D-aspartate (NMDA) receptor agonist, caused cerebral vascular dilation. Dilation of cerebral arterioles to glutamate and cis-ACPD was abolished by chromium mesoporphyrin (CrMP; 10-6 M), a HO inhibitor. In contrast, CrMP did not alter dilation to isoproterenol, a beta -adrenergic receptor agonist. Endothelium-denuded cerebral arterioles did not dilate to glutamate or bradykinin (endothelium-dependent dilator), whereas responses to isoproterenol were preserved. These data indicate that cerebral arterioles from newborn pigs may directly respond to glutamate and the NMDA receptor agonists by endothelium-dependent dilation that involves stimulation of CO production via the HO pathway in the endothelium.

heme oxygenase; endothelial


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