Bradykinin: Difference between revisions
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'''Bradykinin''' is a "nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from [[mast cell]]s during [[asthma]] attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a [[neurotransmitter]].<ref>{{MeSH}}</ref> | '''Bradykinin''' is a "nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from [[mast cell]]s during [[asthma]] attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a [[neurotransmitter]].<ref>{{MeSH}}</ref> | ||
[[ | There are two [[bradykinin receptor]]s. | ||
Bradykinin is degraded by kininase I and kininase II.<ref name="isbn0-07-144040-2p577">{{cite book |author=Ganong, William F. |title=Review of medical physiology |publisher=McGraw-Hill Medical |location= |year=2005 |pages=577 |isbn=0-07-144040-2 |oclc= |doi=}}</ref> Kininase II, formally called [[peptidyl-dipeptidase A]], is the same enzyme as angiotensin converting enzyme. | |||
==Clinical roles== | |||
[[Cough]] when taking [[angiotensin-converting enzyme inhibitor]]s may be due to deficient degradation of bradykinin by kininase II (angiotensin-converting enzyme).<ref name="pmid9791144">{{cite journal |author=Gainer JV, Morrow JD, Loveland A, King DJ, Brown NJ |title=Effect of bradykinin-receptor blockade on the response to angiotensin-converting-enzyme inhibitor in normotensive and hypertensive subjects |journal=N. Engl. J. Med. |volume=339 |issue=18 |pages=1285–92 |year=1998 |month=October |pmid=9791144 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9791144&promo=ONFLNS19 |issn=}}</ref> According to a [[clinical prediction rule]], [[cough]] due to angiotensin-converting enzyme inhibitors is more likely among patients who are "older age, female gender, non-African American (with East Asian having highest risk), no history of previous angiotensin-converting enzyme inhibitor use, and history of cough due to another angiotensin-converting enzyme inhibitor".<ref name="pmid15209608">{{cite journal |author=Morimoto T, Gandhi TK, Fiskio JM, ''et al'' |title=Development and validation of a clinical prediction rule for angiotensin-converting enzyme inhibitor-induced cough |journal=J Gen Intern Med |volume=19 |issue=6 |pages=684–91 |year=2004 |month=June |pmid=15209608 |pmc=1492376 |doi=10.1111/j.1525-1497.2004.30016.x |url=http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0884-8734&date=2004&volume=19&issue=6&spage=684 |issn=}}</ref> | |||
[[Hereditary angioedema]] may be due to unregulated kallikrein activation of bradykinin due to insufficient [[complement C1 inhibitor protein]] (C1 esterase inhibitor)..<ref name="pmid17559913">{{cite journal |author=Schneider L, Lumry W, Vegh A, Williams AH, Schmalbach T |title=Critical role of kallikrein in hereditary angioedema pathogenesis: a clinical trial of ecallantide, a novel kallikrein inhibitor |journal=J. Allergy Clin. Immunol. |volume=120 |issue=2 |pages=416–22 |year=2007 |month=August |pmid=17559913 |doi=10.1016/j.jaci.2007.04.028 |url=http://linkinghub.elsevier.com/retrieve/pii/S0091-6749(07)00864-0 |issn=}}</ref> | |||
==References== | ==References== | ||
<references/> | <references/> | ||
Revision as of 01:34, 16 June 2008
Bradykinin is a "nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.[1]
There are two bradykinin receptors.
Bradykinin is degraded by kininase I and kininase II.[2] Kininase II, formally called peptidyl-dipeptidase A, is the same enzyme as angiotensin converting enzyme.
Clinical roles
Cough when taking angiotensin-converting enzyme inhibitors may be due to deficient degradation of bradykinin by kininase II (angiotensin-converting enzyme).[3] According to a clinical prediction rule, cough due to angiotensin-converting enzyme inhibitors is more likely among patients who are "older age, female gender, non-African American (with East Asian having highest risk), no history of previous angiotensin-converting enzyme inhibitor use, and history of cough due to another angiotensin-converting enzyme inhibitor".[4]
Hereditary angioedema may be due to unregulated kallikrein activation of bradykinin due to insufficient complement C1 inhibitor protein (C1 esterase inhibitor)..[5]
References
- ↑ Anonymous (2024), Bradykinin (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Ganong, William F. (2005). Review of medical physiology. McGraw-Hill Medical, 577. ISBN 0-07-144040-2.
- ↑ Gainer JV, Morrow JD, Loveland A, King DJ, Brown NJ (October 1998). "Effect of bradykinin-receptor blockade on the response to angiotensin-converting-enzyme inhibitor in normotensive and hypertensive subjects". N. Engl. J. Med. 339 (18): 1285–92. PMID 9791144. [e]
- ↑ Morimoto T, Gandhi TK, Fiskio JM, et al (June 2004). "Development and validation of a clinical prediction rule for angiotensin-converting enzyme inhibitor-induced cough". J Gen Intern Med 19 (6): 684–91. DOI:10.1111/j.1525-1497.2004.30016.x. PMID 15209608. PMC 1492376. Research Blogging.
- ↑ Schneider L, Lumry W, Vegh A, Williams AH, Schmalbach T (August 2007). "Critical role of kallikrein in hereditary angioedema pathogenesis: a clinical trial of ecallantide, a novel kallikrein inhibitor". J. Allergy Clin. Immunol. 120 (2): 416–22. DOI:10.1016/j.jaci.2007.04.028. PMID 17559913. Research Blogging.