Where it comes from
- Made in
- Gut and brain neurons making the gamma splice form, one of the two commonest splice forms of the gene
- Sent out by
- With substance P and neurokinin A
- Acts on
- Gut and airway smooth muscle
What it does
- Contracts gut and airway like neurokinin A, and in human bronchus more strongly than any other tachykinin 1
- Longer-lasting than neurokinin A, and found in rat tissue mostly already cut down to a nine-residue fragment 3
- Three splice forms of one gene give substance P with or without these extended peptides 2
In medicine
- No medicine copies it or blocks it. The NK2 blockers act at its receptor, though in human bronchus it works through a binding site that behaves unlike the standard NK2 1
- It is not measured in practice, and most of what tissue holds is a shortened fragment, which complicates any attempt to measure the intact peptide 3
Beyond the body’s own use
- Nothing containing it is in trials, approved or obtainable outside the laboratory
- Its distinguishing fact is potency in human tissue: on isolated human bronchus it contracts more strongly than substance P or neurokinin A, through a site the usual NK2 blockers fit poorly 1
- What is unknown is how much of that is the peptide and how much its slow breakdown. If the extended form is the real agonist in human airway, the NK2 story may have been tested with the wrong ligand 2
Sources
- Burcher et al., Neuropeptide gamma, the most potent contractile tachykinin in human isolated bronchus, Neuropeptides 1991
- Takeda et al., Regional distribution of neuropeptide gamma and other tachykinins of the substance P gene, Regulatory Peptides 1990
- Wang et al., Neuropeptide gamma-(1-9), a major product of gamma-preprotachykinin processing in rat tissues, Journal of Neurochemistry 1993
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.