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Article: Kinins and endothelial control of vascular smooth muscle

TitleKinins and endothelial control of vascular smooth muscle
Authors
Issue Date1995
Citation
Annual Review Of Pharmacology And Toxicology, 1995, v. 35, p. 679-705 How to Cite?
AbstractPlasma and vascular kinins stimulate the production of endothelium-derived nitric oxide, prostacyclin and hyperpolarizing factor (which regulates the function of vascular smooth muscle), and endothelial interactions with blood cells. The role of kinins in vasomotion is determined by the rate of production of the peptides by kininogenases and their degradation by kininases, in particular angiotensin-converting enzyme (ACE). Acute increases in plasma kinin levels during excercise or myocardial ischemia indicate that the metabolism of the peptides is fine tuned to the systemic or local metabolic demands. The release of endothelial vasodilators is impaired (or counterbalanced by the release of chemical or functional antagonists) in atherosclerosis, hypertension, diabetes, subarachidonic hemorrhage, and following postischemic injury. ACE-inhibitors potentiate the action of kinins and normalize endothelial function. In septic shock, hypotension triggered by overproduction of kinins leads to cardiovascular impairment and end-organ damage. Thus the balance in the metabolism of kinins modulates the control of blood flow by the endothelium.
Persistent Identifierhttp://hdl.handle.net/10722/171161
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:28Z-
dc.date.available2012-10-30T06:12:28Z-
dc.date.issued1995en_US
dc.identifier.citationAnnual Review Of Pharmacology And Toxicology, 1995, v. 35, p. 679-705en_US
dc.identifier.issn0066-4251en_US
dc.identifier.urihttp://hdl.handle.net/10722/171161-
dc.description.abstractPlasma and vascular kinins stimulate the production of endothelium-derived nitric oxide, prostacyclin and hyperpolarizing factor (which regulates the function of vascular smooth muscle), and endothelial interactions with blood cells. The role of kinins in vasomotion is determined by the rate of production of the peptides by kininogenases and their degradation by kininases, in particular angiotensin-converting enzyme (ACE). Acute increases in plasma kinin levels during excercise or myocardial ischemia indicate that the metabolism of the peptides is fine tuned to the systemic or local metabolic demands. The release of endothelial vasodilators is impaired (or counterbalanced by the release of chemical or functional antagonists) in atherosclerosis, hypertension, diabetes, subarachidonic hemorrhage, and following postischemic injury. ACE-inhibitors potentiate the action of kinins and normalize endothelial function. In septic shock, hypotension triggered by overproduction of kinins leads to cardiovascular impairment and end-organ damage. Thus the balance in the metabolism of kinins modulates the control of blood flow by the endothelium.en_US
dc.languageengen_US
dc.relation.ispartofAnnual Review of Pharmacology and Toxicologyen_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Therapeutic Useen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCardiovascular Diseases - Therapyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKallikrein-Kinin System - Physiologyen_US
dc.subject.meshKinins - Metabolism - Physiology - Therapeutic Useen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth, Vascular - Metabolism - Physiologyen_US
dc.subject.meshPeptidyl-Dipeptidase A - Metabolismen_US
dc.titleKinins and endothelial control of vascular smooth muscleen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1146/annurev.pa.35.040195.003335-
dc.identifier.pmid7598512-
dc.identifier.scopuseid_2-s2.0-0028987882en_US
dc.identifier.volume35en_US
dc.identifier.spage679en_US
dc.identifier.epage705en_US
dc.identifier.isiWOS:A1995QV29100027-
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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