Bradykinin is the main mediator involved in most cases.
Bradykinin lowers blood pressure by causing blood vessel dilation.
In hereditary angioedema, Bradykinin formation is caused by continuous activation
Platelets release other proinflammatory factors like serotonin, Bradykinin, prostaglandins, prostacyclins,
An injection of a medicine which blocks Bradykinin, such as icatibant.
thereby increasing the breakdown of Bradykinin, which increases the risk of developing hypertension.
Both of these reduce catecholamine sensitivity, increase Bradykinin and nitric oxide, improving arterial functioning(39).
Symptoms are due to excess Bradykinin, but they develop the condition rather than inheriting it.
Lanadelumab is a fully human monoclonal
antibody that targets kallikrein and prevents the production of Bradykinin.
It should be remembered that valsartan is not an AT1 receptor agonist and does
not inhibit angiotensin-converting enzyme(kinase II), which neutralizes Bradykinin.
In hereditary angioedema, Bradykinin formation is caused by continuous activation
of the complement system due to a deficiency in one of its prime inhibitors, C1-esterase(aka: C1-inhibitor or C1INH), and continuous production of kallikrein,
Mechanisms contributing to blood-brain barrier dysfunction include physical disruption by arterial hypertension or trauma, and tumor-facilitated release of vasoactive and endothelial destructive compounds e.g. arachidonic acid, excitatory neurotransmitters,
eicosanoids, Bradykinin, histamine, and free radicals.