Oxytocin structure. Inset shows oxytocin bound to neurophysin

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Oxytocin

Oxytocin is a mammalian hormone that in women is released mainly after stimulation of the nipples or distention of the vagina and that facilitates birth and breastfeeding. It is also released during orgasm in both sexes. In the brain, it acts as a neurotransmitter and is involved in bonding and the formation of trust between people. more...

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Synthetic oxytocin is sold as medication under the trade names Pitocin and Syntocinon and also as generic Oxytocin.

Synthesis, storage and release

Oxytocin is made in magnocellular neurosecretory cells in the supraoptic nucleus and paraventricular nucleus of the hypothalamus and is released into the blood from the posterior lobe of the pituitary gland. Oxytocin is also made by some neurons in the paraventricular nucleus that project to other parts of the brain and to the spinal cord.

In the pituitary gland, oxytocin is packaged in large, dense-core vesicles, where it is bound to neurophysin as shown in the inset of the figure; neurophysin is a large peptide fragment of the giant precursor protein molecule from which oxytocin is derived by enzymatic cleavage.

Secretion is regulated by the electrical activity of the oxytocin cells in the hypothalamus. These cells generate action potentials that propagate down axons to the neurosecretory nerve endings in the pituitary; the endings contain large numbers of oxytocin-containing vesicles, which are released by exocytosis when the terminals are depolarised.

Structure and relation to vasopressin

Oxytocin is a peptide of nine amino acids (a nonapeptide). The sequence is cysteine - tyrosine - isoleucine - glutamine - asparagine - cysteine - proline - leucine - glycine (CYIQNCPLG). The cysteine residues form a sulfur bridge.

Oxytocin has a molecular mass of 1007 daltons. One international unit (IU) of oxytocin is the equivalent of about 2 micrograms of pure peptide.

The structure of oxytocin is very similar to that of vasopressin, which is also a nonapeptide with a sulfur bridge. Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons can make corticotropin-releasing hormone (CRH) and vasopressin neurons dynorphin, for example, that act locally. The magnocellular neurons that make oxytocin are adjacent to magnocellular neurons that make vasopressin, and are similar in many respects.

Oxytocin and vasopressin were discovered, isolated and synthesized by Vincent du Vigneaud in 1953, work for which he received the Nobel Prize in Chemistry in 1955.

The oxytocin receptor is a G-protein-coupled receptor which requires Mg²⁺ and cholesterol. It belongs to the rhodopsin-type (class I) group of G-protein-coupled receptors.

Actions

Oxytocin has peripheral (hormonal) actions, and also has actions in the brain.

Peripheral (hormonal) actions

The peripheral actions of oxytocin mainly reflect secretion from the pituitary gland. Oxytocin receptors are expressed by the myoepithelial cells of the mammary gland, and in both the myometrium and endometrium of the uterus at the end of pregnancy. In some mammals, oxytocin receptors are also found in the kidney and heart.

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Does use of oxytocin and dinoprostone inserts shorten labor more than use of oxytocin after removal of dinoprostone? - Patient-Oriented Evidence that Matters
From Journal of Family Practice, 5/1/02 by Jessica Kill

Christensen FC, Tehranifar M, Gonzalez JL, Qualls CR, Rappaport VJ, Rayburn WF. Randomized trial of concurrent oxytocin with a sustained release dinoprostone vaginal insert for labor induction at term. Am J Obstet Gynecol 2002; 186:61-5.

* BACKGROUND Simultaneous use of oxytocin and prostaglandin E2 preparations may offer a more efficient approach to labor induction by shortening the induction to delivery time. However, the manufacturer of sustained-release dinoprostone inserts warns against concurrent use with oxyytocin since the risks of uterine hyperactivity and complications are unknown. This study compared the use of oxytocin immediately after placement of a sustained-release dinoprostone insert with delayed use of oxytocin after removal of dinoprostone.

* POPULATION STUDIED The study included 71 women who presented to the University of New Mexico Health Sciences Center with indications for labor induction, singleton gestations with cephalic presentation, intact membranes, reactive nonstress tests, no previous uterine surgery, and unfavorable cervices (Bishop score [greater than or equal to] 6). These patients are similar to those encountered in a primary care setting. Women with vaginal bleeding, more than 2 contractions in 10 minutes, asthma, known hypersensitivity to prostaglandins, or conditions that would contraindicate the induction of labor were excluded.

* STUDY DESIGN AND VALIDITY Women were randomly assigned (concealed allocation assignment) to either low-dose oxytocin infusion (2 mU/min with 2-mU/min increases every 20 minutes, up to a maximum dose of 36 mU/min) started either 10 minutes after placement of a 10-mg sustained-release dinoprostone insert (immediate group) or 30 minutes after the removal of the insert (delayed group). Inserts were left in place for 12 hours if possible. The exact time of dioprostone insert placement into the posterior fornix was recorded. Evaluation of the cervix and Bishop scoring were performed prior to placement and immediately following removal of the insert. Two investigators blinded to group assignment monitored tracings of contractions.

The study included patients who in clinical practice are candidates for induction therapy, and was powered to detect a 6-hour difference in induction to delivery times. However, the sample size was too small to detect differences in morbidities such as difference in cesarean delivery and uterine hyperstimulation. Analysis by intention to treat was not performed. Three women were excluded from the final statistical analysis for protocol violation, no delivery data, and withdrawal of consent.

* OUTCOMES MEASURED The primary outcome measured was the time from induction to delivery. Secondary outcomes included changes in cervical score at 12 hours, frequency of deliveries within 24 hours, incidence of uterine hyperstimulation, rate of cesarean deliveries, and maternal and neonatal complications.

* RESULTS The mean induction to delivery time was 972 minutes in the immediate group versus 1516 minutes in the delayed group (P = .001). The change in Bishop score at the time of the insert removal was significantly greater in the immediate oxytocin group as compared with the delayed oxytocin group (P = .01). Immediate versus delayed administration of oxytocin increased the likelihood of delivery within 24 hours of induction (90% vs 53%, respectively; P = .002). No cases of hyperstimulation syndrome occurred with the immediate group versus 3 cases in the delayed group (P = .24). Cesarean delivery rates were similar (16% vs 13% for the immediate and delayed groups, respectively; P = .73), and cesarean deliveries were needed only in nulliparous women. No women developed intrapartum chorioamnionitis, and 1 woman in each group developed postpartum endometritis. Neonatal Apgar scores measuring less than 7 at 5 minutes were similar between groups (0% vs 6% for the immediate and delayed groups, respectively; P = .49).

RECOMMENDATIONS FOR CLINICAL PRACTICE

Concurrent administration of oxytocin and sustained-release dinoprostone (prostaglandin) reduced the time from induction, to delivery compared to oxytocin after removal of dinoprostone. This study found no increased risk of adverse events with concurrent administration. However, caution should be applied when using this concurrent therapy regimen until maternal and neonatal safety has been properly evaluated with larger studies.

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