Response of Ovine Uterine Arteries to Nerve Stimulation After Perfusions of Prostaglandin F2a, Norepinephrine or Neurotransmitter Antagonists1

Abstract

The role of ovarian steroids and prostaglandin F2.alpha. (PGF2.alpha.) in regulating constriction of ovine uterine arteries was studied. Unilaterally ovulating ewes [5] were sacrificed on each of days 0 (estrus) 3, 6 and 10 of the estrus cycle. A segment of uterine artery supplying each horn was removed, cannulated and subjected to 10 min perfusions of saline (control vehicle), PGF2.alpha., norepinephrine (NE) and neurotransmitter antagonists. At the end of each perfusion vasoconstriction was provoked by stimulation of periarterial sympathetic nerves. Ovaries having greatest follicular development (follicular ovaries) contained a corpus luteum in 16 of 20 ewes. Regardless of stage studied, uterine arteries adjacent to follicular ovaries (ipsilateral arteries) responded to nerve stimulation (NS) with increased constriction compared to low consistent responses of contralateral arteries. Ipsilateral arterial response to NS following saline, PGF2.alpha. or NE infusions increased from day 0 to 10 of the cycle. Perfusion of NE increased constriction of ipsilateral arteries to NS at each stage studied (P < 0.01); PGF2.alpha. only enhanced constriction of ipsilateral arteries of day-10 ewes (P < 0.01). Phentolamine reduced constriction (P < 0.01) of ipsilateral arteries to NS. Subsequent ipsilateral arterial perfusion with PGF2.alpha. failed to increase vasoconstriction to NS over that exhibited following phentolamine. Repeated ipsilateral arterial perfusion with NE after PGF2.alpha. resulted in a return of vasoconstriction to NS (P < 0.01) in spite of intervening propranolol or atropine perfusions. Blood flow to each uterine horn of the ewe possibly is controlled by local ovarian steroids and PGF2.alpha. concentrations acting in concert to regulate the release of neurotransmitter and thus the extent of vasoconstriction.