The control of uterine smooth muscle remains a major challenge for clinicians, affecting preterm deliveries, dysfunctional labour and post-partum haemorrhage. The task for physiologists is to gain a better understanding of the mechanisms that lead to myometrial contractility and thus help identify novel therapeutic targets. Calcium is a key to uterine contractility and thus understanding the changes in it, at the global and local level is important.

An advantage for studies of uterine physiology is the availability of both well characterized animal models and human tissue from women undergoing caesarean section operations. In addition tissues from patients who have for example diabetes or are obese or are expecting twins, allows insight into how the normal physiology of the myometrium may be altered. I will present data that sheds light on Ca signalling in the myometrium. This will include work we have done to elucidate the role of the sarcoplasmic reticulum in the uterus and its contribution to contraction and excitability. I will then show data from studies of women with altered myometrial function due to disease, lifestyle and multiple pregnancy. In my summary I will relate these findings to our knowledge of physiology and make suggestions as to how these data may be translated for patient benefit. I will also show how our knowledge of the uterus has evolved over the millennia.