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>
[[Angiotensin-converting enzyme inhibitor]]s also decrease the degradation of bradykinin.<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> This may contribute to some patients having a cough when taking angiotensin-converting enzyme inhibitors. 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>


There are two [[bradykinin receptor]]s.
There are two [[bradykinin receptor]]s.

Revision as of 22:58, 15 June 2008

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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 cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.[1]

Angiotensin-converting enzyme inhibitors also decrease the degradation of bradykinin.[2] This may contribute to some patients having a cough when taking angiotensin-converting enzyme inhibitors. 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".[3]

There are two bradykinin receptors.

References