Брадикинин

Amorphous solid.

Bradykinin is used to lower blood pressure, increase bradykinin (by inhibiting its degradation) further lowering blood pressure. Bradykinin dilates blood vessels via the release of prostacyclin, nitric oxide, and endothelium-derived hyperpolarizing factor.

ChEBI: A linear nonapeptide messenger belonging to the kinin group of proteins, with amino acid sequence RPPGFSPFR. Enzymatically produced from kallidin in the blood, it is a powerful vasodilator that causes smooth muscle contraction, and may mediate inflammation

The kallikrein–kinin system is an enzymatic pathway giving rise to two predominant vasoactive peptides, kallidin and bradykinin. Kallikrein, the enzyme responsible for the formation of these peptides, exists in plasma and tissues. However, circulating levels of the end products, kallidin and bradykinin, are quite low because the kallikrein enzymes are present largely in inactive forms. In addition, the short half-life of these peptides (15 seconds) also contributes to low plasma levels. In general, the kinins produce relaxation of vascular smooth muscle and vasodilation. Bradykinin causes vascular smooth muscle relaxation by stimulating the endothelium to release prostacyclin and nitric oxide. Blood flow to the brain, heart, viscera, skeletal muscle, and glands is increased. In nonvascular smooth muscle, bradykinin will produce a contractile response.
Other actions of kinins include activation of clotting factors simultaneously with the production of bradykinin. In the kidney, bradykinin production results in an increase in renal papillary blood flow, with a secondary inhibition of sodium reabsorption in the distal tubule. In the peripheral nervous system, bradykinin is important for the initiation of pain signals. It is also associated with the edema, erythema, and fever of inflammation.
Bradykinin exerts its physiological effects via two receptors, the B1 and B2 receptors, with most of its physiological effects being mediated by the B2 receptor. The precise function of the B1 receptor is unclear; however, some of the chronic inflammatory responses to bradykinin may be mediated through actions at this receptor.
Bradykinin antagonists of the B2 receptor are currently in development and may find utility in the treatment of pain associated with burns and such chronic inflammatory disorders as arthritis, asthma, and chronic pain.

Induces the release of nitric oxide. Other physiological functions include stimulation of pain receptors, inhibition of cAMP accumulation, induction of smooth muscle contraction, and vasodilation. Also involved in edema resulting from trauma or injury. Improves post-ischemic recovery of heart via a nitric oxide-dependent mechanism.

Powerful vasodilator; increased capillary permeability; stimulates pain receptors; contraction of smooth muscle; teratogen; mutagenic.

9-peptide, produced in response to tissue damage, inflammation, viral infections, etc. Produces pain, increased vascular permeability, and synthesis of prostaglandins.