Book chapter
4 - Biology of Cerebral Vascular Muscle
Primer on Cerebrovascular Diseases, pp.13-16
Academic Press
1997
DOI: 10.1016/B978-012743170-3.50005-4
Abstract
This chapter summarizes the current evidence regarding mechanisms which account for activation of guanylate cyclase, adenylate cyclase, and potassium channels in cerebral vascular muscle. This chapter also focuses on endothelium-dependent relaxation and mechanism of vasomotor regulation. Two forms of guanylate cyclase are present in vascular muscle and contribute to regulation of vascular tone. The first form of guanylate cyclase is soluble, or cytosolic, and the second form is particulate (associated with the plasma membrane). Formation of nitric oxide occurs in cerebral blood vessels under basal conditions and activity of nitric oxide synthase can be further stimulated by increases in intracellular calcium that occur in response to receptor mediated agonists like acetylcholine or in response to increases in shear stress. After release by endothelium, nitric oxide diffuses to vascular muscle and stimulates soluble guanylate cyclase, resulting in a rise in intracellular concentrations of cyclic GMP and relaxation. Under normal conditions, nitric oxide is released both lumenally and ablumenally by endothelium. Release of nitric oxide into the vascular lumen contributes to the antithrombogenic properties of endothelium because nitric oxide inhibits aggregation of platelets and adherence of leukocytes to endothelium.
Details
- Title: Subtitle
- 4 - Biology of Cerebral Vascular Muscle
- Creators
- Frank M. Faraci - University of IowaDonald D. Heistad - University of Iowa
- Resource Type
- Book chapter
- Publication Details
- Primer on Cerebrovascular Diseases, pp.13-16
- DOI
- 10.1016/B978-012743170-3.50005-4
- Publisher
- Academic Press
- Language
- English
- Date published
- 1997
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984303998602771
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