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Related to Kinins: Prostaglandins, Cytokines


Any of various structurally related polypeptides, such as bradykinin, that act locally to induce vasodilation and contraction of smooth muscle.

[Short for bradykinin.]


1. (Biochemistry) any of a group of polypeptides in the blood that cause dilation of the blood vessels and make smooth muscles contract
2. (Botany) another name for cytokinin
[C20: from Greek kin(ēma) motion + -in]


(ˈkaɪ nɪn, ˈkɪn ɪn)

2. any of a group of hormones, formed in body tissues, that cause dilation of blood vessels.
[1950–55; (cyto) kin (esis) + -in1]
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.kinin - any of a class of plant hormones that promote cell division and delay the senescence of leaves
growth regulator, phytohormone, plant hormone - (botany) a plant product that acts like a hormone
References in periodicals archive ?
Inflammation itself arises from myriad etiologic pathways, with multiple inflammatory mediators potentially involved, including histamines, cytokines, eicosanoids (for example, prostaglandins, thromboxanes, and leukotrienes), complement cascade components, kinins, fibrinopeptide enzymes, nuclear factor-kappa B, and free radicals.
The data with aprotinin elsewhere fully support for the elevation of endogenous kinins by BT venom.
Kinins and cytokines in plasma and cerebrospinalfluid of patients with neuropsychiatric lupus.
20] Apart from the described clinical pathophysiology, the underlying cause to the symptoms are mediated by an elaborate confluence of multiple cytokines, such as interleukin (IL-1[beta]), TNF-[alpha], and IL-6; prostaglandins, kinins, acute phase proteins, and various proteins of the complement system like C5a which help shaping the immune response in its totality.
Kinins have functions such as the provision of cardiovascular balance and the formation of an inflammatory response (2).
Cathepsin K targets kinins that are involved in bone resorption, but it is expressed in other tissues as well, and it may target other classes of kinins.
The first phase is mediated through release of histamine, serotonin and kinins, whereas the second phase is related to the release of prostaglandin-like substances which peak at 3 hours.
The inflammatory pain results from activation of resident cells such as mast cells, infiltration of inflammatory cells such as neutrophils, and the release of inflammatory mediators such as kinins, amines, prostanoids, growth factors and cytokines.
Increase in kinins on post-exercise hypotension in normotensive and hypertensive volunteers.
It is speculated that the pain is due to formation of kinins, including bradykinin.
sup][20] Kinins that derived from KNG involved in cell proliferation, leukocyte activation, cell migration, endothelial cell activation, and nociception.