ArticleAmerican journal of physiology. Heart and circulatory physiology2007
Carbon monoxide and Ca2+-activated K+ channels in cerebral arteriolar responses to glutamate and hypoxia in newborn pigs.
Article in American journal of physiology. Heart and circulatory physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- On the mechanisms of brain blood flow regulation during hypoxia.The Journal of physiology · 2025Pooled it
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Impact of acute and chronic hypoxia on the heme oxygenase/carbon monoxide pathway in naked mole-rats (Heterocephalus glaber).The Journal of experimental biology · 2025Article
- Regulation of the Cerebral Circulation During Development.Comprehensive Physiology · 2021Article
- The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020Review
- The Role of Astrocytes in the Central Nervous System Focused on BK Channel and Heme Oxygenase Metabolites: A Review.Antioxidants (Basel, Switzerland) · 2019Review
- Hydrogen sulfide activates Ca²⁺ sparks to induce cerebral arteriole dilatation.The Journal of physiology · 2012Article
- Carbon monoxide as an endogenous vascular modulator.American journal of physiology. Heart and circulatory physiology · 2011Review
- Interactions between adenosine and K+ channel-related pathways in the coupling of somatosensory activation and pial arteriolar dilation.American journal of physiology. Heart and circulatory physiology · 2010Article
- Time-dependent action of carbon monoxide on the newborn cerebrovascular circulation.American journal of physiology. Heart and circulatory physiology · 2010Article
- Potassium channels and neurovascular coupling.Circulation journal : official journal of the Japanese Circulation Society · 2010Review
- Molecular investigations of BK(Ca) channels and the modulatory beta-subunits in porcine basilar and middle cerebral arteries.Journal of molecular histology · 2009Article
- Article
- Role of heme oxygenase-2 in pial arteriolar response to acetylcholine in mice with and without transfusion of cell-free hemoglobin polymers.American journal of physiology. Regulatory, integrative and comparative physiology · 2008Article
- The RCK1 high-affinity Ca2+ sensor confers carbon monoxide sensitivity to Slo1 BK channels.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Cerebroprotective functions of HO-2.Current pharmaceutical design · 2008Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Large-conductance calcium-activated potassium (K(Ca)) channels regulate the physiological functions of many tissues, including cerebrovascular smooth muscle. l-Glutamic acid (glutamate) is the principal excitatory neurotransmitter in the central nervous system, and oxygen tension is a dominant local regulator of vascular tone. In vivo, glutamate and hypoxia dilate newborn pig cerebral arterioles, and both dilations are blocked by inhibition of carbon monoxide (CO) production. CO dilates cerebral arterioles by activating K(Ca) channels. Therefore, the present study was designed to investigate the effects of glutamate and hypoxia on cerebral CO production and the role of K(Ca) channels in the cerebral arteriolar dilations to glutamate and hypoxia. In the presence of iberiotoxin or paxilline that block dilation to the K(Ca) channel opener, NS-1619, neither CO nor glutamate dilated pial arterioles. Conversely, neither paxilline nor iberiotoxin inhibited dilation to acute severe or moderate prolonged hypoxia. Both glutamate and hypoxia increased cerebrospinal fluid (CSF) CO concentration. Iberiotoxin that blocked dilation to glutamate did not attenuate the increase in CSF CO. The guanylyl cyclase inhibitor, 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ), which blocked dilation to sodium nitroprusside, did not inhibit dilation to hypoxia. These data suggest that dilation of newborn pig pial arterioles to glutamate is mediated by activation of K(Ca) channels, consistent with the intermediary signal being CO. Surprisingly, although 1) heme oxygenase (HO) inhibition attenuates dilation to hypoxia, 2) hypoxia increases CSF CO concentration, and 3) K(Ca) channel antagonists block dilation to CO, neither K(Ca) channel blockers nor ODQ altered dilation to hypoxia, suggesting the contribution of the HO/CO system to hypoxia-induced dilation is not by stimulating vascular smooth muscle K(Ca) channels or guanylyl cyclase.
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Registered trials
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