Despite an impressive amount of effort and extensive research, our knowledge of parturition remains scant. Although numerous scientists have investigated “the timing of birth”, we still have a limited understanding of the biological mechanisms that control events initiating delivery, or the availability of methods supposed to prevent these mechanisms from acting inappropriately. A multitude of factors and structures are involved; the myometrium, cervix, placenta and the fetus must act in concert to assure successful delivery. We do know that achievement of a “perfect” contractile force is not the sole factor. Successful delivery is also impacted by subtle differences in pelvic shape or size.

The length of mammalian pregnancy is tightly regulated to assure the delivery of a newborn mature enough to survive the extra-uterine environment. A successful pregnancy requires near complete relaxation of the uterus for more than ninety-five percent of gestation, overcoming the inherent tendency of the myometrium to contract with stretch. This active and highly regulated process is called myometrial quiescence. It requires not only the near absence of myometrial contractions, but also its refractoriness to contractile agents.

Oxygen radicals and reactive oxygen species are normal attributes of aerobic life. In most molecules, the electrons are paired and, with the exception of hydrogen, the four outer most pairs of each atom form chemical bonds. Electrons are in a relatively stable energy state when paired. A free radical is a molecule with an unpaired electron. Free radicals of oxygen are of particular importance to living organisms in which they are involved in the genesis of a wide array of diseases and physiological processes (e.g. life span and ageing).

The cardiovascular system undergoes profound changes during pregnancy. Maternal intravascular volume begins to increase in the first trimester rising an average of 45% by term.1 Cardiac output increases similarly2 and is redistributed to organs whose functions are crucial for a successful pregnancy. In the guinea pig, uterine artery (UA) blood flow increases 3500%, while mesenteric and renal artery blood flows increase only 90% and 10% respectively.3 Blood flow to the trunk actually diminishes. The mechanism underlying this redistribution is unknown. Coupled with the rise in cardiac output is a decrease in the systemic pressor response to angiotensin II (AII), norepinephrine(NE), and epinephrine.4–8 There is also a decrease in the contraction response among some but not all vascular beds. For example, contraction of UA to NE and thromboxane is characteristically reduced by pregnancy, whereas the response of the carotid artery is unaltered8–10 Since pregnancy does not alter neuroeffector mechanisms of NE such as release, receptor sensitivity, and accumulation11, changes in sympathetic control during pregnancy must be dependent on alterations at sites other than the neuroeffector junction. We have hypothesized that the mechanisms which alter vascular reactivity during pregnancy also mediate the redistribution of maternal cardiac output.9 We have further hypothesized that many of these mechanisms involve endothelium-dependent factors which are modulated by sex hormones.