Biology Reference
In-Depth Information
Chapter 42
Ion Channel Assessment
Marcel Alexander Kamp , Hans-Jakob Steiger , and Daniel Hänggi
Abstract
Molecular mechanisms underlying subarachnoid hemorrhage (SAH)-induced cerebral vasospasm are
complex and still partially unknown. Molecular-biological studies and clinical trials support a central
role of ion channels, but further detailed studies have to evaluate their exact role during vasospasm
following SAH.
This chapter focuses on methods and principles of ion channel assessment which includes the
wide-spread spectrum of molecular-biological, electrophysiological, immunochemical, and functional
methods.
Key words:
Ion channel, Calcium channels, Vasospasm, Subarachnoid hemorrhage
1. Introduction
and Background
Cellular mechanisms following SAH leading to cerebral vasospasm
are still part of discussion. Elevation of cytoplasmatic calcium (Ca
2+
)
was considered to be one major factor causing SAH-related vasos-
pasm as well as inhibition of Ca
2+
sparks and increase of the Ca
2+
sensitivity of the contractile apparatus (
1-3
). Membranous ion
channels are mainly involved in ion maintenance of the cell.
Therefore, different ion channels have shown to contribute to the
development of cerebral vasospasm following SAH: in general,
oxy-hemoglobin leads to a decrease of functional potassium chan-
nels (K
v
) in the plasma membrane and to their suppression by
enhanced tyrosine kinase activity (
4, 5
). Furthermore, Ca
2+
infl ux
through voltage-gated Ca
2+
channels (Ca
v
) contributes to cerebral
vasospasm which leads to the assumption that L-type Ca
2+
channel
blockers are strongly effective to treat vasospasm. Besides L-type
Ca
2+
channels, it was documented that other subtypes of voltage-
gated ion channels play a role in the cellular mechanism of arterial
contraction.
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