Regulation of Na+, K+‐ ATPase by cardiotonic steroids: Participation in the sodium theory for migraine
Abstract
Abstract Background The sodium theory for migraine proposes that excessive sodium pumping into the cerebrospinal fluid (CSF) leads to sodium infiltration into the neural tissue, which can lead to activation and central sensitization of trigeminovascular neurons, predisposing individuals to migraine. Dysregulation of the Na+, K+‐ATPase pump in the choroid plexus is likely to be the primary cause of elevated sodium in the CSF. The identity of intrinsic regulatory molecules that are inhibitors for this pump and their involvement in migraine have been the subject of numerous studies; however, data detailing the involvement of only a few of these regulatory molecules in migraine pathology are published. The regulation mechanisms and the path for these regulators are currently unknown. Objective This review aims to present data supporting the sodium theory for migraine and explore potential mechanisms for brain sodium dysregulation. Methods PubMed, Google Scholar, and UniProtKB/Swiss‐Prot were searched for articles and corroborating information through March 2024. Search items for PubMed and Google Scholar included headache, migraine, Na+, K+‐ATPase, cardiotonic steroids, ouabain, digoxin, bufalin, marinobufagenin, telocinobufagin, organic anion transporters, and ATP‐binding cassette transporters. The Human Protein Atlas was used to obtain receptor and transporter expression levels. Results Clinical and preclinical studies reveal that dysregulation of Na+, K+‐ATPase in the choroid…
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