Abstract
The gas, carbon monoxide (CO), is produced physiologically by catabolism of heme to CO, free iron, and biliverdin.1 This reaction is catalyzed by heme oxygenase with reduction of NADPH. Heme oxygenase (HO) is expressed as three known iso-forms that are attached to the endoplasmic reticulum by a hydrophobic sequence near the carboxy terminus of the protein:1 the easily inducible HO-1, the constituitively expressed poorly inducible HO-2 and a third isoform with much lower heme degrading activity.2CO can be a vascular paracrine factor. HO-1 and HO-2 have been identified in vascular endothelial and smooth muscle cells, with HO-2 being constituitively expressed.1,3,4,5 HO-2 is expressed in highest concentration in the brain5,9 where it resides in neurons, vascular endothelium and smooth muscle.1,6 CO can cause increases in cGMP in both autocrine and paracrine fashions3,7,8,9 and can hyperpolarize vascular smooth muscle via modification of a histidine residue on the external membrane side of the large conductance Ca activated potassium channel (Kca).9,10,11 By either of these mechanisms CO could cause endothelial independent dilation of arteries and arterioles.
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© 2002 Springer Science+Business Media New York
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Leffler, C.W., Jaggar, J.H., Fan, Z. (2002). Co and Neonatal Cerebral Circulation. In: Abraham, N.G. (eds) Heme Oxygenase in Biology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0741-3_9
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DOI: https://doi.org/10.1007/978-1-4615-0741-3_9
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