In women, relaxin is secreted into the circulation by the corpus luteum in the ovary. During pregnancy it is also released from the placenta, the membranes which surround the foetus, and the lining of the uterus. In men, relaxin is secreted from the prostate gland and can be detected in the semen, but is not generally found in the blood circulation.
The effects of relaxin are most well-described during the female reproductive cycle and pregnancy. Relaxin levels in the circulation rise after ovulation, during the second half of the menstrual cycle. At this stage it is thought to relax the wall of the uterus by inhibiting contractions, and it also prepares the lining of the uterus for pregnancy. If pregnancy does not occur, relaxin levels drop again. During pregnancy, relaxin levels are at their highest in the first trimester. At this time it is believed to promote implantation of the developing foetus into the wall of the uterus and the growth of the placenta. Early in pregnancy, relaxin also inhibits contractions in the wall of the uterus, to prevent premature childbirth. Relaxin can regulate the mother’s cardiovascular and renal systems to help them adapt to the increase in demand for oxygen and nutrients for the foetus, and to process the resulting waste products. It is thought to do this by relaxing the mother’s blood vessels to increase blood flow to the placenta and kidneys.
Towards the end of pregnancy relaxin promotes rupture of the membranes surrounding the foetus and the growth, opening and softening of the cervix and vagina to aid the process of childbirth. There is also some evidence that relaxin can relax the ligaments at the front of the pelvis to ease delivery of the baby. There are several other factors involved in labour, but the exact trigger remains unclear.
The role of relaxin in men is less clear. However, there is evidence that it may increase the movement of sperm cells in the semen.
Relaxin belongs to the same family of hormones as insulin. Over the last decade, several relaxin-like peptides have been discovered, although the function of these peptides remains unclear.
Recent studies have revealed effects of relaxin on other systems in the body. Relaxin decreases tissue fibrosis in the kidney, heart, lungs and liver, and promotes wound healing. Tissue fibrosis is the formation of hard tissue as a result of inflammation which can lead to scarring and loss of organ function. This has made relaxin of interest to scientists studying how the heart heals after it has been damaged, which may help to treat heart failure in the future. In addition, relaxin can influence blood pressure by relaxing blood vessels; promote the growth of new blood vessels; and is also anti-inflammatory. All of these properties could make it a potential therapeutic target for the treatment of certain diseases.
The control of relaxin release in humans is not fully understood. It is believed that relaxin production by the ovary during the menstrual cycle is stimulated by luteinising hormone from the pituitary gland, and that its release during pregnancy is also stimulated by human chorionic gonadotrophin from the placenta. It remains unclear whether relaxin can feed back to the pituitary or the foetus to affect luteinising hormone or human chorionic gonadotrophin levels and so control its own release.
Relaxin carries out its actions on the reproductive system and other organs by activating specific receptors on these tissues.
Disorders of relaxin secretion have not been described in detail. Studies have suggested that high levels of circulating relaxin in the mother are associated with premature birth, presumably via its effects on the rupture of the foetal membranes and the opening of the cervix. However, further research is needed to confirm these findings.
There is some evidence that low levels of relaxin may contribute to a condition known as scleroderma, where the skin thickens and hardens. This is caused by the development of fibrosis and scarring on the skin, which also occurs in the lung, stomach and blood vessels.
Last reviewed: Mar 2015