NK

(redirected from Neurokinin)
Also found in: Medical, Acronyms.

NK

(histology)
References in periodicals archive ?
SP binds to neurokinin receptors (NK) 1 and 2 of enteric cholinergic secretomotor neurons in submucosal ganglia.
Neurokinin B (endogenous ligand of TACR3) is involved in pathogenesis of Parkinson's disease by interacting with brain dopaminergic transmission [19].
The other two members are simply called neurokinin A and neurokinin B.
The wide variety of drugs in development includes opioid receptor ligands, bradykinin antagonists, mPGES-1 inhibitors, glutamate receptor antagonists, substance P and neurokinin receptor antagonists, norepinephrine transporter inhibitors,P2X2 neuron receptor antagonists and nitric oxide-based analgesics.
Finally, part three presents three case studies: T-type calcium channel and glycine transporter type 1 inhibitors, bioisosteric replacements for the neurokinin 1 receptor, and neuronal nitric oxide synthase inhibitors.
Quantification of neuropeptides (calcitonin gene-related peptide, substance P, neurokinin A, neuropeptide Y and vasoactive intestinal polypeptide) expressed in healthy and inflamed human dental pulp.
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.
Targeting the neurokinin receptor 1 with aprepitant: A novel antipruritic strategy.
Quantitative analysis of substance P, neurokinin A and calcitonin gene-related peptide in pulp tissue from painful and healthy human teeth.
Substance P induces vomiting and binds to neurokinin 1 (NK-1) receptors in the abdominal vagus, the nucleus tractus solitarius, and the area postrema.
PGE2 stimulates the release of tachykinins, which stimulate neurokinin receptors on afferent nerves and the detrusor smooth muscle and as a result promote detrusor contraction (Andersson & Hedlund, 2002; Verhamme et al.
For OIH, proposed mechanisms include a role for glutaminergic activation (also implicated in tolerance), altered opioid intracellular signalling involving G protein-coupled receptor switching, a role for substance P and neurokinin 1 (NK-I) receptors and spinal dynorphin and, finally, increasing evidence implicating Toll-like receptor (TLR) signalling and glial cells.