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1 Veterinary Physiology & Pharmacology, Texas A&M University, College Station, TX, USA
* To whom correspondence should be addressed. E-mail: jstallone{at}cvm.tamu.edu.
To determine the roles of estrogen and constrictor prostanoids in vasopressin (VP)-induced contraction of the female (F) rat aorta, vascular reactivity to VP was determined in thoracic aortas of intact (InT), ovariectomized (OvX) and OvX + estradiol-replaced (OvX+ER) F rats in the presence of indomethacin (Indo), NS-398, SQ 29,548 (SQ) or vehicle-control. The effects of estrogen on vascular reactivity to the thromboxane analog U-46619 were also examined. Maximal contractile response to VP in InT-F rats (5,567 ± 276 mg/mg ring wt.) was markedly attenuated by OvX (2,485 ± 394 mg, P < 0.001), and restored by ER with 17
-estradiol (5,059 ± 194 mg, P > 0.1). Indo and NS-398 significantly attenuated maximal responses to VP in InT-F rats to a similar extent (3,176 ± 179 mg, P < 0.0001 and 3,258 ± 152 mg, P < 0.0001, respectively). OvX abolished and ER restored the inhibitory effects of Indo, NS-398, and SQ. Contractile responses of rat aorta to U-46619 were significantly greater (P < 0.0001) in F (5,040 ± 238 mg) than in males (3,679 ± 96 mg). OvX markedly attenuated (3,923 ± 84 mg, P < 0.01) and ER restored (5,024 ± 155 mg, P > 0.1) responses to U-46619 in F aorta. These data reveal that estrogen is an important regulator of the contractile responses of the F rat aorta to VP, which appears to potentiate both COX-2 and constrictor prostanoid function in the vascular wall.
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