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

Departments of Animal Science, Oregon State University Corvallis, Oregon 97331
Departments of Pharmacology, Oregon State University Corvallis, Oregon 97331

Abstract

The role of ovarian steroids and prostaglandin F₂ (PGF₂) in regulating constriction of ovine uterine arteries was studied. Five unilaterally ovulating ewes were sacrificed on each of days 0 (estrus), 3, 6 and 10 of the estrous cycle. A segment of uterine artery supplying each horn was removed, cannulated and subjected to 10-min perfusions of saline (control vehicle), PGF₂, norepinephrine (NE) and neurotransmitter antagonists. At the end of each perfusion, vasoconstriction was provoked by stimulation of periarterial sympathetic nerves. Ovaries having the 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 the low consistent responses of contralateral arteries. Responses of ipsilateral arteries to NS following perfusions of saline, PGF₂ or NE 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), while PGF₂ 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 perfusion of ipsilateral arteries with PGF₂ failed to increase vasoconstriction to NS over that exhibited following phentolamine. Repeated perfusion of ipsilateral arteries with NE after PGF₂ resulted in a return of vasoconstriction to NS (P < 0.01) in spite of intervening perfusions of propranolol or atropine. It is proposed that blood flow to each uterine horn of the ewe is controlled by local concentrations of ovarian steroids and PGF₂ acting in concert to regulate the release of neurotransmitter and thus the extent of vasoconstriction.

Footnotes

¹ Technical Paper No. 4401, Oregon Agricultural Experimental Station.

Received November 10, 1976.

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