# Situation: A 24-year-old primigravida at 39 weeks' gestation comes to a lying-in clinic at 02:00 because of abdominal tightening since midnight. Her membranes are intact, she has no vaginal bleeding, and she reports active fetal movement. Her prenatal course has been uncomplicated. While waiting, the client asks why labor starts at the end of pregnancy. Among the proposed mechanisms of labor onset, the functional withdrawal of which hormone is believed to remove the main inhibition of uterine contractions?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=629374  
> language: ko  
> subject: Nursing Practice II — Maternal and Child Health Nursing

## 문제

Situation: A 24-year-old primigravida at 39 weeks' gestation comes to a lying-in clinic at 02:00 because of abdominal tightening since midnight. Her membranes are intact, she has no vaginal bleeding, and she reports active fetal movement. Her prenatal course has been uncomplicated.

While waiting, the client asks why labor starts at the end of pregnancy. Among the proposed mechanisms of labor onset, the functional withdrawal of which hormone is believed to remove the main inhibition of uterine contractions?

## 보기

1. Progesterone **✔ 정답**
2. Estrogen
3. Oxytocin
4. Prostaglandin

**정답: 1**

## 해설

Progesterone maintains uterine quiescence during pregnancy. A functional withdrawal of its effect near term, together with a rising estrogen effect, prostaglandins, and oxytocin, is among the proposed mechanisms of labor onset. The exact trigger in humans is not fully known, but progesterone is the hormone that inhibits contractions.

## 심화 해설

Why labor begins near term

The question asks which hormone, when its effect is “functionally withdrawn” at the end of pregnancy, removes the main brake on uterine contractions. The answer is progesterone.

Progesterone is the dominant hormone that maintains uterine quiescence throughout pregnancy. It suppresses myometrial excitability, reduces gap junction formation, and inhibits the expression of contraction-associated proteins. Near term, the myometrium becomes less responsive to progesterone even though the circulating level does not drop in humans. This phenomenon is called functional progesterone withdrawal [1][2][3].

A key point for licensure exams is the contrast between humans and most other mammals. In many animals, labor is preceded by a sharp fall in maternal progesterone concentration. In humans, however, maternal, fetal, and amniotic fluid progesterone concentrations remain elevated up to and during labor [3][4]. Therefore, the trigger is not a numerical decrease in the hormone level but a loss of its biological effect at the tissue level.

Several mechanisms have been proposed to explain this functional withdrawal. They include changes in the relative expression of progesterone receptor isoforms, altered regulation of progesterone-responsive genes through nuclear factor kappaB (NF-kB) promoter sites, and non-genomic actions of progesterone [1]. Epigenetic regulation of progesterone receptors has also been implicated in shifting the myometrium from a quiescent to a contractile state [3].

Watch out! Do not confuse the hormone that maintains pregnancy with the hormones that actively drive contractions. Oxytocin and prostaglandins promote uterine contractions, and estrogen enhances myometrial excitability and oxytocin receptor expression. They all rise or become more effective near term, but the question asks which hormone’s withdrawal removes the main inhibition. That is progesterone.

Key point! The exact trigger of human labor remains incompletely understood, but the proposed framework is that a functional loss of progesterone action, combined with rising estrogen, prostaglandin, and oxytocin effects, shifts the uterus from quiescence to coordinated contractions [1][2][4].

The table below summarizes the roles of the four hormones in labor onset.

| Hormone | Role in pregnancy and labor | Change near term in humans |
| --- | --- | --- |
| Progesterone | Maintains uterine quiescence; inhibits contractions | Circulating level stays high; tissue responsiveness decreases (functional withdrawal) |
| Estrogen | Promotes myometrial excitability; increases oxytocin receptors and gap junctions | Effect increases relative to progesterone |
| Oxytocin | Stimulates rhythmic uterine contractions | Receptor sensitivity increases near term |
| Prostaglandin | Promotes cervical ripening and myometrial contraction | Production increases near term |

In this client’s clinical picture—term primigravida with intact membranes, no bleeding, active fetal movement, and abdominal tightening since midnight—the nurse can explain that the onset of labor reflects a shift in the hormonal balance that has maintained the pregnancy. The functional withdrawal of progesterone is the central event that removes the primary inhibition of uterine contractions [1][2][3][4].References (research sources)

- [1]The involvement of progesterone in the onset of human labour.Research articleAstle S, Slater DM, Thornton S (2003) · DOI: 10.1016/s0301-2115(02)00422-0

- [2]Myometrial progesterone responsiveness and the control of human parturition.Research articleMesiano S (2004) · DOI: 10.1016/j.jsgi.2003.12.004

- [3]Epigenetic regulation of progesterone receptors and the onset of labour.Research articleIlicic M, Zakar T, Paul JW (2019) · DOI: 10.1071/RD18392

- [4]Progesterone receptor profile in the decidua and fetal membrane.Research articleGoldman S, Shalev E (2007) · DOI: 10.2741/2088

## 임상 시나리오

Labor Onset: Functional Progesterone WithdrawalWhy the uterus stops being quiet at term
Progesterone is the dominant hormone maintaining uterine quiescence during pregnancy. It suppresses myometrial excitability, reduces gap junction formation, and inhibits contraction-associated proteins. Near term, the myometrium becomes less responsive to progesterone even though circulating levels do not drop in humans—this is called functional progesterone withdrawal.

In most other mammals, labor is preceded by a sharp fall in maternal progesterone concentration. In humans, maternal, fetal, and amniotic fluid progesterone levels remain elevated up to and during labor. The trigger is therefore not a numerical decrease but a loss of biological effect at the tissue level.

Proposed mechanisms include changes in the relative expression of progesterone receptor isoforms, altered regulation of progesterone-responsive genes through NF-kB promoter sites, and non-genomic actions of progesterone. Rising estrogen effect, prostaglandins, and oxytocin then work together to promote contractions once the progesterone brake is removed.

CautionDo not confuse functional withdrawal with a measured drop in serum progesterone. In humans, serum progesterone remains elevated during labor, so ordering a progesterone level to predict or confirm labor onset is not clinically useful.

## 핵심 개념

- **Functional progesterone withdrawal** — Loss of myometrial responsiveness to progesterone near term despite stable circulating levels, removing the main inhibition of uterine contractions.
- **Uterine quiescence** — The state of relative myometrial inactivity maintained throughout pregnancy, primarily by progesterone.
- **Contraction-associated proteins** — Proteins such as gap junctions and oxytocin receptors whose expression increases near term to promote uterine contractility.
- **Myometrial excitability** — The readiness of uterine smooth muscle to depolarize and contract, suppressed by progesterone during pregnancy.
- **Gap junction formation** — Intercellular channels between myometrial cells that allow synchronized contractions; inhibited by progesterone and increased by estrogen near term.

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