Differential vascular reactivity of fetal and maternal placental arteries from melatonin treated nutrient‐restricted sheep to endothelium‐dependent and independent vasodilators

Abstract

Maternal nutrient restriction and decreased scotophase concentrations of melatonin have been associated with severely compromised pregnancies. We hypothesized that melatonin supplementation during a compromised pregnancy will improve the maternal (CAR) and fetal (COT) placental vascular reactivity thereby ensuring sufficient umbilical blood flow to the developing fetus. Pregnant ewes (n=32) were fed a control (ADQ) or nutrient restricted diet (RES) supplemented with (MEL) or without 5mg melatonin (CON) from day 50–130 of gestation. The sodium nitroprusside (SNP)‐induced relaxation of isolated CAR and COT arteries did not differ significantly between treatment groups. Independent of the maternal nutrition status, the sensitivity to bradykinin (BK) induced relaxation of COT but not CAR arteries, increased significantly (p<0.05) in MEL group. Moreover, CAR arteries showed increased sensitivity to BK‐induced relaxation, irrespective of the nutrition restriction, compared to COT arteries (pD2= 7.46 ± 0.1 CAR Vs 6.94 ± 0.2 COT). The norepinephrine and angiotensin II induced contraction of CAR and COT arteries did not differ significantly between treatment groups. The increased sensitivity of COT arteries to BK‐induced relaxation in MEL groups represents an important mechanism by which dietary melatonin supplementation improves the umbilical blood flow and placental nutrient transfer capacity.