Alterations in vascular smooth muscle contractility during ovine pregnancy

During pregnancy, sheep develop attenuated systemic and uterine vascular responsiveness to α-adrenergic stimulation. To determine whether this reflects altered vascular smooth muscle function, we studied the responsiveness of smooth muscle isolated from systemic and uterine arteries to KCl and phenylephrine. Uterine, renal, and carotid arteries were collected from nonpregnant, pregnant (131 ± 2 days, ± SD), and late postpartum (144 ± 4 days) ewes; endothelium was removed and open rings were hung for measurement of isometric force. There were no differences in concentration-response relationships nor maximal stresses generated to phenylephrine between nonpregnant, pregnant, and late postpartum states for carotid or renal arteries. However, the 50% maximal concentration for phenylephrine of uterine arteries in the nonpregnant state (2.8 ± 0.9 x 10^-6 M) was greater than the pregnant state (0.76 ± 0.05 x 10^-6 M). Moreover, uterine arteries from pregnant sheep generated significantly more stress than those from nonpregnant sheep (2.2 ± 0.23 vs. 0.73 ± 0.23 x 10⁶ dyn/cm², P < 0.01). The attenuated systemic and uterine vascular responses associated with pregnancy do not result from diminished adrenergic sensitivity or contractile capability of arterial smooth muscle. In contrast, there is increased stress-generating capacity of uterine arterial smooth muscle during pregnancy, which is reversed during the postpartum period.