tachykinin

(redirected from Tachykinins)

tach·y·ki·nin

(tak'i-kī'nin),
Any member of a group of polypeptides, widely scattered in vertebrate and invertebrate tissues, which have in common four of the five terminal amino acids: Phe-Xaa-Gly-Leu-Met-NH2; pharmacologically, they all cause hypotension in mammals, contraction of gut and bladder smooth muscle, and secretion of saliva.
[G. tachys, swift, + kineō, to move, + -in]

tachykinin

/tachy·ki·nin/ (-ki´nin) any of a family of peptides structurally and functionally similar to substance P; all are potent, rapidly acting secretagogues and cause smooth muscle contraction and vasodilation.

tachykinin

tachykinin

(tăk″kī′nĭn) [″ + ″],

TK

Any of a large family of peptides that function as neurotransmitters in the central and peripheral nervous systems. They have extraneuronal activity in other body tissues. Their diverse biological actions are mediated through cellular G proteins.
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References in periodicals archive ?
Several studies have reported that inflammation processes in the TMJ cause the production of proinflammatory substances, including tachykinins such as substance P and calcitonin gene-related peptides (CGRPs) (17).
7] Poor gut contractility and slow intestinal transit times in ICU patients also involve inhibitory neurotransmitters such as nitric oxide and vasoactive intestinal peptide, as well as tachykinins such as substance P and the neurokinin family.
4) Additional brain stress response systems involve the signalingmolecules norepinephrine, neuropeptide y, tachykinins, anddynorphins.
One important mechanism is by an increase of tachykinins in patient blood, possibly mediated by neurotrophins produced in response to viral infection.
Distribution and colocalization of calcitonin gene-related peptide, tachykinins, and vasoactive intestinal peptide in normal and idiopathic unstable human urinary bladder.
Airway hyperresponsiveness induced by chronic exposure to cigarette smoke in guinea pigs: role of tachykinins.
In addition, ACE has other potential substrates, including tachykinins, neurotensin substance P, and others.
The ARBs were developed to overcome several of the deficiencies of ACE inhibitors: competitive inhibition of ACE results in a reactive increase in renin and angiotensin I levels, which may overcome the blockade effect; ACE is a relatively nonspecific enzyme that has substrates in addition to angiotensin I, including bradykinin and other tachykinins, and thus, inhibition of ACE may result in accumulation of these substrates; production of angiotensin II can occur through non-ACE pathways as well as through the primary ACE pathway, and these alternative pathways are unaffected by ACE inhibition; specific adverse effects are associated with ACE inhibitor effects on the enzyme; and ARBs may offer more complete angiotensin II inhibition by interacting selectively with the receptor site (1).
Tachykinins are neurohormones that, among other activities, control contraction and relaxation of smooth muscles such as those in the blood vessels.