Abstract |
This review describes the ability of certain diseases, such as essential hypertension, atherosclerosis, angina, and vasospasm, to reduce vascular nitric oxide (NO) formation or to increase its metabolism. In contrast, others, such as hypotension, sepsis, stroke, myocardial depression, and inflammatory responses, increase NO synthesis. The mechanism implicated in the changes in the formation and metabolism of NO are described. To prevent or treat these pathological processes, in which a deficiency in vascular NO formation plays a causative role, NO may be provided through methods such as direct NO administration or indirect NO supply through either NO donors or L-arginine, which facilitates NO formation.
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Authors | J Marín, M A Rodríguez-Martínez |
Journal | Pharmacology & therapeutics
(Pharmacol Ther)
Vol. 75
Issue 2
Pg. 111-34
(Aug 1997)
ISSN: 0163-7258 [Print] England |
PMID | 9428001
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Nitric Oxide
- Arginine
- Nitric Oxide Synthase
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Topics |
- Animals
- Arginine
(therapeutic use)
- Arteriosclerosis
(metabolism)
- Cardiovascular Diseases
(drug therapy, metabolism)
- Diabetes Mellitus
(metabolism)
- Endothelium, Vascular
(metabolism)
- Humans
- Hypertension
(metabolism)
- Nitric Oxide
(biosynthesis, physiology, therapeutic use)
- Nitric Oxide Synthase
(physiology)
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