Biological effects of bradykinin

The first and perhaps most important function of plasma kininogens is the delivery of BK, a potent biologically active peptide. BK itself is a potent stimulator of endothelial cell synthesis of prostacyclin and nitric oxide formation (both vasodilators and inhibitors of platelet function), phagocyte superoxide formation, tissue plasminogen activator release and endothelial cell-dependent smooth muscle hyper-polarization factor formation. When vessels are injured, BK stimulates protein kinase C and subsequently MAP kinase, which can result in vascular smooth muscle growth and proliferation. However, when vessels are intact, BK appears to prevent vascular muscle growth and proliferation, thus keeping blood flow and vessels patent. These actions of BK are mediated through a constitutive hepta-spanning G protein-coupled receptor known as the B2 receptor. A receptor called the B1 receptor is induced by inflammatory cytokines and binds des Arg9-BK but its function is not yet clear.

BK plays a role in blood pressure regulation although little is known about what regulates its liberation from kininogens by tissue kallikreins. Transgenic mice overexpressing tissue kallikrein are hypotensive and lose the diurnal fluctuation of blood pressure. Intramuscular delivery of rat kallistatin, a naturally occurring serine proteinase inhibitor, reverses hypotension in transgenic mice overexpressing human tissue kallikrein. Gene delivery of tissue kallikrein reduces mean blood pressure of spontaneous hypertensive rats and this inhibition is blocked by kallistatin. These molecular genetic studies directly indicate that presumed tissue kallikrein-induced bradykinin liberation directly modifies local and potentially systemic blood pressure regulation.

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