During Ovine fetal development systemic vascular SM demonstrates age-dependent rises in actin, myosin heavy chain (MHC) and 204 kD MHC-isoform(l) and a fall in MHC-B, a nonmuscle MHCI. Relationships between these alterations and stress generation are unknown. The umbilical circulation is known to respond to several agonists and is crucial in fetal growth and well-being, but SM protein expression in UA SM is not described. We thus hypothesized that compared to fetal systemic vascular SM, UA SM functionally and biochemically resembles adult SM. To examine this we studied femoral arteries (FA) and abdominal aorta (Ao) from near-term fetal (130-145d; term 145d) and adult sheep and external (EUA) and intra-abdominal (IUA) UA. Actin/MHC contents (μg/mg of wet weight) and MHCI were measured by SDS-PAGE using 3-20% and 4% gels, respectively. 200 kD MHCI were measured by Western analysis. Stress (104 N/m2) was measured in vascular strips stimulated by 10-6M phenylephrine and/or 65mM KCI. Results(Xbar±SEM; differing superscripts in rows indicate p<0.01, ANOVA):Table Only fetal FA and Ao were unresponsive to all agonists and expressed MHC-B by Western analysis. In near-term fetal sheep, FA and Ao are functionally immature as assessed by absent stress generation and MHC-B expression, while UA are unique to the fetal vasculature, resembling adult arteries in both protein expression and capacity to contract. Thus, consistent with in vivo studies, UA SM may actively modulate fetal blood pressure, distribution of cardiac output and tissue oxygen delivery, while systemic arteries passively distribute blood flow.

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