Cookies Policy

This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies.

I accept this policy

Find out more here

Pathophysiological activities of the kallikrein-kinin system with emphasis on the cardiovascular disorders

No metrics data to plot.
The attempt to load metrics for this article has failed.
The attempt to plot a graph for these metrics has failed.
The full text of this article is not currently available.

Brill’s MyBook program is exclusively available on BrillOnline Books and Journals. Students and scholars affiliated with an institution that has purchased a Brill E-Book on the BrillOnline platform automatically have access to the MyBook option for the title(s) acquired by the Library. Brill MyBook is a print-on-demand paperback copy which is sold at a favorably uniform low price.

Access this article

+ Tax (if applicable)
Add to Favorites
You must be logged in to use this functionality

Recent evidence suggests an important role for the kallikrein-kinin system in the pathophysiology of hyperalgesia, arthritis, inflammatory bowel disease, pancreatitis, asthma and endotoxemia. In fact, hyperactivity of kinins can be considered as pro-inflammatory because of their ability to cause all the cardinal signs of inflammation directly activating their B1 and B2 receptors. Kinins are also able to release other potent inflammatory mediators. In endotoxemia, excessive kinin release may account for inducing severe life threatening hypotension. Several specific kinin receptor antagonists are being developed with the major interest in treating these pathological conditions to block the activation of kinin receptors. Furthermore, kallikrein inhibitors may have a role in the treatment of arthritis and inflammatory gut diseases to block the excessive release of kallikrein. On the other side, all the components of the kallikrein-kinin system are located in the vascular smooth muscle as well as in the heart. From numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction and left ventricular hypertrophy, it can be assumed that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular related diseases. The ability of kallikrein gene delivery to produce a wide spectrum of beneficial effects makes it an excellent candidate in treating hypertension, cardiovascular and renal diseases. In addition, stable kinin agonists may also be available in the future as therapeutic agents for cardiovascular and renal disorders.


Full text loading...


Data & Media loading...

Article metrics loading...



Can't access your account?
  • Tools

  • Add to Favorites
  • Printable version
  • Email this page
  • Subscribe to ToC alert
  • Get permissions
  • Recommend to your library

    You must fill out fields marked with: *

    Librarian details
    Your details
    Why are you recommending this title?
    Select reason:
    Inflammopharmacology — Recommend this title to your library
  • Export citations
  • Key

  • Full access
  • Open Access
  • Partial/No accessInformation