The ductus venosus is weakly responsive to prostaglandin E2 (PGE<sub>2</sub>) and prostacyclin (PGI<sub>2</sub>) which behave as vasodilators. This influence is lost with the improved pulmonary clearance resulting from the absence of an umbilical blood supply. This loss of blood supply also causes the sphincter in the ductus venosus to constrict thereby diverting blood to the liver. Closure of the ductus venosus becomes permanent after two to three weeks. The remnants of the ductus venosus form the ligamentum venosum.
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The ductus venosus is weakly responsive to prostaglandin E2 (PGE<sub>2</sub>) and prostacyclin (PGI<sub>2</sub>) which behave as vasodilators. This influence is lost with the improved pulmonary clearance resulting from the absence of an umbilical blood supply. This loss of blood supply also causes the sphincter in the ductus venosus to constrict thereby diverting blood to the[[Liver - Anatomy & Physiology|liver]]. Closure of the ductus venosus becomes permanent after two to three weeks. The remnants of the ductus venosus form the ligamentum venosum.