Sexual dimorphism in prostanoid-potentiated vascular contraction: roles of endothelium and ovarian steroids

Abstract

The effects of constrictor prostanoid (CP) pathway inhibitors on vascular reactivity to vasopressin (VP) and phenylephrine (PE) were examined in thoracic aortas of male, female, and ovariectomized (OVX) female Sprague-Dawley rats. Maximal contractile response of control (Cont) aortas to VP was markedly higher in females (3,885 ± 332 mg/mg ring wt) than in males (810 ± 148 mg). Indomethacin (Indo; 10 μM) attenuated maximal response to VP in females (3,043 ± 277 mg) but not in males. SQ-29,548 (SQ; 1 μM) attenuated maximal response to VP in females (3,042 ± 290 mg) to a similar extent as Indo. Dazoxiben (Daz; 10 μM) alone had no effect, but Daz + SQ attenuated maximal contractile response to VP to a similar extent as SQ alone. Removal of the endothelium in female aortas attenuated contractile responses to VP in Cont aortas. OVX attenuated maximal contractile response to VP in Cont aortas (2,093 ± 329 mg) and abolished the attenuating effects of Indo. Indo, SQ, and Daz exerted identical effects on contractile responses of male, female, and OVX female aortas to PE. These findings establish the following in the rat aorta: 1) CP, probably thromboxane and/or endoperoxide, is responsible for ∼25–30% of contractile responses of females, but not males, to VP and PE; 2) CP production by the female aorta is primarily endothelial in origin; and 3) ovarian steroids modulate production and/or actions of CP in female aortas.