Uterine Contraction - Anatomy & Physiology

Myometrial Contraction

• Myometrium consists of:
  • Non-striated smooth muscle fibres
  • Nerves, Blood and Lymph

• During pregnancy, Oestrogens stimulate muscle cell hypertrophy.
• Myometrial cells behave as a functional syncytium, being electrically coupled via specialised regions of contact known as gap junctions/nexi.
• The combination of the above factors allows strong, coordinated myometrial contraction.

• Excitation of smooth muscle depends on alteration in membrane potential. Myometrial cells must be depolarised (-50mV) to achive contraction.
• Spontaneous depolarizing pacemaker potentials occur. If the magnitude of these exceeds the critical threshold, a burst of action potentials will fire.
• This causes calcium influx from endoplasmic reticular stores and extracellular fluid.
• Intracellular calcium binds to regulatory sites on actin and myosin, allowing expression of ATPase, thus causing contraction.

• Uterine contractions increase in both frequency and amplitude during labour. This causes an increase in uterine pressure from 10mmHg to 50-100mmHg.

The Birth Canal

Brachystasis

• Myometrial cells contract and shorten, but do not regain their original length upon relaxation.
• Reduces the uterine volume and causes retraction of the lower uterine segment and the cervix to create a birth canal.

Retraction Ring

• The Uterus is divided into two segments:
  • Upper segment: contractile
  • Lower segment: passive
• The junction between these segments is the retraction ring.
• Palpation of the retraction ring is used as an indicator of progression through labour.

Endocrine Control

Schematic Diagram to show the Endocrine Influence on Myometrial Contraction,Copyright RVC 2008

• Two hormones directly regulate myometrial contractions:
  • Oxytocin: from the posterior pituitary gland (not the corpus luteum) lowers the excitation threshold of muscle cells to increase the likelihood of action potential firing. Oxytocin also stimulates prostaglandin release.
    • The uterine Oxytocin receptor is a G protein coupled receptor with a Gαq subinit. Thus the signalling pathway is via a calcium second messenger. Hence prostaglandin and oxytocin are complementory in action.
  • Prostaglandins: Stimulate liberation of calcium from intracellular stores to cause the rise in intracellular calcium concentration required for myometrial contraction.