Estrogen-induced pial arteriolar dilation is prostanoid associated in the newborn

Estrogens have vascular protective effects in addition to their anti-lipid effects, Estrogens enhance endothelium-dependent vasodilation in the adult. While estrogens increase constitutive nitric oxide (NO) synthase activity, NO does not have a major role in maintenance of vasomotor tone in the newborn. We hypothesized that if estrogens altered vascular tone in the newborn, it would be via a dilator system other than NO. Using the closed cranial window technique, pial arterial vessel diameter was quantified in response to topically administered ovarian steroids in piglets anesthetized with α-chloralose. 17β-estradiol (10 ^-5M) produced pial vasodilation that was not altered by topical LNA(10 ^-3M) and was attenuated by indomethacin (5mg/kg iv): 36.1±1.6% vs 27.3±6.1% vs 6.4±2.6% respectively. 17α-estradiol (10 ^-5M) produced pial vasodilation that was not altered by topical LNA and was attenuated by indomethacin: 34.6±2.2% vs 26.2±4.2% vs 3.3±4.2% respectively. Carbacyclin(6·10M ^-11), a prostacyclin analogue in a concentration not sufficient to alter pial diameter, was able to restore the dilator response to β-estradiol attenuated by indomethacin. We conclude that in the newborn the estradiols produce a prostanoid associated pial vasodilation with no major role for NO, and that the prostanoids play a permissive role in the response.