Reproductive function is highly dependent on levels of both neurokinin B and also the G-protein coupled receptor ligand kisspeptin.

[2] The first NKB studies done attempted to resolve why high levels of the peptide may be implicated in pre-eclampsia during pregnancy.

This subpopulation is targeted by many steroid hormones and works to form a network that feeds back to GnRH pulse generator.

The NK3R receptor group when activated with a synthetic agonist of NKB, senktide, has been shown to stimulate the secretion of luteinizing hormone.

Additional NK3R receptors have also been found in various other places in the body including: uterus, mesenteric vein, gut neurons, and placenta.

The kisspeptin, neurokinin B, and dynorphin cell groups are found to be co-localized to more than 95% of all of the aforementioned receptors in the arcuate nucleus.

[4] These findings are important since GnRH release plays such a pivotal role in regulating hormonal control in the bodies of humans.

Pre-eclampsia is a disorder found in around 5% of pregnant women, usually presenting in the 37th week of gestation, with prognosis ranging from mild to severe.

This can result in a number of problems for the fetus including poor growth, lack of amniotic fluid, and placental abruption.

Research indicates that the tachykinin peptide neurokinin B may play a role, as placental expression of the TAC3 gene, which codes for NKB, was found in high levels in women with pre-eclampsia.

Additional studies done on rodents introduced to high levels of NKB indicated the vasoregulatory properties of the peptide, such as the vasoconstriction found in cases of pre-eclampsia.

However, it seems as though depending on which receptor NKB binds, the peptide can cause both constriction and dilation of the blood vessels.

By injecting NKB analogs pulsatile GnRH was secreted, activating the hypothalmic-pituitary axis and therefore releasing LH.