Capillary endothelial Na(+), K(+), ATPase transporter homeostasis and a new theory for migraine pathophysiology.
Headache
; 50(3): 459-78, 2010 Mar.
Article
em En
| MEDLINE
| ID: mdl-19845787
ABSTRACT
BACKGROUND:
Cerebrospinal fluid sodium concentration ([Na(+)](csf)) increases during migraine, but the cause of the increase is not known.OBJECTIVE:
Analyze biochemical pathways that influence [Na(+)](csf) to identify mechanisms that are consistent with migraine.METHOD:
We reviewed sodium physiology and biochemistry publications for links to migraine and pain.RESULTS:
Increased capillary endothelial cell (CEC) Na(+), K(+), -ATPase transporter (NKAT) activity is probably the primary cause of increased [Na(+)](csf). Physiological fluctuations of all NKAT regulators in blood, many known to be involved in migraine, are monitored by receptors on the luminal wall of brain CECs; signals are then transduced to their abluminal NKATs that alter brain extracellular sodium ([Na(+)](e)) and potassium ([K(+)](e)).CONCLUSIONS:
We propose a theoretical mechanism for aura and migraine when NKAT activity shifts outside normal limits (1) CEC NKAT activity below a lower limit increases [K(+)](e), facilitates cortical spreading depression, and causes aura; (2) CEC NKAT activity above an upper limit elevates [Na(+)](e), increases neuronal excitability, and causes migraine; (3) migraine-without-aura may arise from CEC NKAT over-activity without requiring a prior decrease in activity and its consequent spreading depression; (4) migraine triggers disturb, and treatments improve, CEC NKAT homeostasis; (5) CEC NKAT-induced regulation of neural and vasomotor excitability coordinates vascular and neuronal activities, and includes occasional pathology from CEC NKAT-induced apoptosis or cerebral infarction.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Artérias Cerebrais
/
ATPase Trocadora de Sódio-Potássio
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Células Endoteliais
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Transtornos de Enxaqueca
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article