Mutations in the C1 inhibitor gene can cause hereditary angioedema, a genetic condition resulting from reduced regulation of bradykinin by C1-INH.
42.
Under physiological conditions the enzyme reaches about 60 % of its maximal activity toward angiotensin I while it reaches its full activity toward bradykinin.
43.
Similar to KLKB1, three tissue kallikreins KLK1, KLK2 and KLK12 also participate in regulation of blood pressure via the activation of bradykinin.
44.
The inactivation of bradykinin and the conversion of angiotensin I to angiotensin II in the lungs was thought to be caused by the same enzyme.
45.
Several blood-borne substances, such as a few types of prostaglandins, leukotrienes, serotonin and bradykinin, are excreted through the lungs.
46.
Bradykinin is also thought to be the cause of the dry cough in some patients on angiotensin-converting enzyme ( ACE ) inhibitor drugs.
47.
Overactivation of bradykinin is thought to play a role in a rare disease called hereditary angioedema, formerly known as hereditary angio-neurotic edema.
48.
Plasma kallikrein liberates kinins ( bradykinin and kallidin ) from the kininogens, peptides responsible for the regulation of blood pressure and activation of inflammation.
49.
Neurturin has been shown to upregulate B1 ( bradykinin ) receptors in neurons of mice, indicating a possible influence on pain and inflammation pathways.
50.
Polymorphisms in ACE or aminopeptidase P ( APP ), another enzyme responsible for bradykinin degradation ( 20 % ) may also contribute to HTRs.
