Biology Reference
In-Depth Information
Chapter 43
Biochemical Assessments of Cerebral Vasospasm:
Measurement of cGMP, PKC, and PTK in Cerebral Arteries
Masayo Koide and Shigeru Nishizawa
Abstract
Cerebral arterial tone is regulated by a concert of contractile signals [e.g., increased intracellular Ca
2+
,
protein kinase C (PKC) activation], and vasodilatory signals [e.g., increased cyclic guanosine monophos-
phate (cGMP)] in arterial smooth muscle cells. After subarachnoid hemorrhage (SAH), a variety of
molecules are released into subarachnoid space and stimulate arterial cells to enhance contractile signals
and/or attenuate vasodilatory signals, resulting in a severe constriction in cerebral arteries called cerebral
vasospasm. Previous studies suggest increased PKC and protein tyrosine kinase (PTK) activity as well as
decreased cGMP signaling may contribute to the development of cerebral vasospasm following SAH.
Here, we describe approaches to examine these intracellular signaling molecules, PKC (isoforms), PTK,
and cGMP, in cerebral arteries from a dog SAH model.
Key words:
Cyclic guanosine monophosphate, Protein kinase C, Isoforms, Protein tyrosine kinase,
Cerebral artery, Subarachnoid hemorrhage
1. Introduction
The arterial wall consists of three layers; endothelium, smooth
muscle media, and tunica adventitia. Smooth muscle media con-
tains primarily smooth muscle cells that contract or relax, altering
arterial diameter. The endothelium is single layer of vascular
endothelial cells, which are known to produce many vasoactive
substances, resulting in smooth muscle contraction (endothelium
derived contracting factors; EDCFs, e.g., endothelin-1 (
1
)) or
dilation (endothelium-derived relaxing factors; EDRFs, e.g., nitric
oxide (NO) (
2, 3
), prostacyclin (
4
)). Tunica adventitia contains
many cell types (e.g., fi brobrasts, mast cells, and perivascular nerves)
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