Comparison of the effects of neuropeptide K and neuropeptide γ with neurokinin A at NK2 receptors in the hamster urinary bladder

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Abstract
Neuropeptide K (NPK) and neuropeptide γ (NPγ) are two endogenous N-terminally extended forms of neurokinin A (NKA). Here, we compared their effects with those of NKA on 125I-NKA binding, phosphatidyl-inositol (PI) turnover and smooth muscle contraction in the hamster urinary bladder. NPK, NPγ and NKA were equipotent in competing 125I-NKA from NK2 receptors in crude hamster bladder membranes. All three peptides stimulated PI turnover by approximately 750% with similar potency. In a third series of experiments, these peptides had similar efficacy in inducing a dose-dependent contraction of bladder smooth muscle. The NK2 receptor selective antagonist L-659,877 (cyclo[Leu-Met-Gln-Trp-Phe-Gly]) inhibited the stimulation of PI turnover and bladder contractions induced by all three tachykinins. The present results show that NKA, NPK and NPγ display a similar biological profile. The N-terminal extensions of NPK and NPγ appear not to influence binding of these peptides to NK2 receptors, NK2 receptor mediated stimulation of PI turnover, or smooth muscle contraction in hamster urinary bladder.