Akinin is any of various structurally relatedpeptides, such asbradykinin andkallidin.[1] They are members of theautacoid family.[2] Kinins are peptides that are cleaved from kininogens by the process ofkallikreins. Kallikreins activate kinins when stimulated.[3]
It is a component of thekinin-kallikrein system.
Their precursors arekininogens.[4] Kininogens contain a 9-11 amino acid bradykinin sequence.[5]
Inbotany, theplant hormones known ascytokinins were first called kinins; the name was changed to avoid confusion.[6]
Kinins are short-lived peptides that causepain sensation, arteriolar dilation, increasevascular permeability, and causecontractions insmooth muscle. Kinins transmit their effects throughG protein-coupled receptors.[5]
Kinins act onaxons to blocknerve impulses, which leads to distal muscle relaxation. They are also potent nerve stimulators which are mostly responsible for the pain sensation (and sometimesitching). Kinins increase vascular permeability by acting on vascularendothelial cells to cause cell contraction. Concomitantly, they induce local expression of adhesive molecules. Together they increasewhite blood cell adhesion andextravasation. Kinins are rapidly inactivated by theproteases generated locally during the aforementioned processes.[7]
They act locally to inducevasodilation and contraction of smooth muscle.[8] Kinins function as mediators forinflammatory responses by triggering theimmune system. They are also able to regulatecardiovascular andrenal (kidney) function by mediating the effects ofACE inhibitors.[9] Reduced kinin activity can result inhigh blood pressure,sodium retention, and the narrowing of blood vessels.[3]
Aspirin inhibits the activation of kallenogen by interfering with the formation of the kallikreinenzyme, which is essential in the process of activation.
Kinins are mostly produced at inflamed or injuredtissues of the body and humanbody fluids. Kinin peptides (kallidin and bradykinin) are located in humanblood andurine.[10]
There are two types of kinin receptors: B1 and B2. Both are G-protein coupled receptors in which B2 are expressed in various tissues and B1 are induced from inflammation, tissue injuries, and stress.[11] The human body contains more B2 receptors than B1 receptors.[10]
B1 and B2 receptors are essentially related ashomologous genes.[12] Both have the same cellular signaling pathways, although their patterns are different in intensity and duration; the B1 signaling pathway lasts longer than the B2 signaling pathway.[13]
Kinin was initially discovered by J.E. Abelous and E. Bardier in 1909 while performing experiments where human body fluids, such as urine, were injected into dogs. The resulting observations state that the urine caused a reduction in blood pressure.[3][clarification needed]
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