Abstract
The present study was designed to test the hypothesis that nicotine exposure increases vascular contractility and decreases endothelium-dependent relaxation of pregnant uterine arteries (UAs). UAs were isolated from near-term pregnant ewes. Arteries were subjected to nicotine treatment for a short-term of 20 min or a long-term of 48 h. Agonist-induced contractions and relaxations were measured in tissue baths. Endothelial cells were isolated from the UAs and eNOS was detected with Western blotting and immunohistochemistry. Nicotine produced a doses-dependent increase in phenylephrine (PE)-induced contractions after long-term, but not short-term, treatment. Pretreatment of vessels with L-NNA significantly increased PE-induced contractions, which were abolished after chronic nicotine treatment. Chronic but not acute nicotine treatment significantly attenuated A23187-induced relaxations of UAs. Unlike A23187, endothelium-independent relaxations mediated by SNP were not altered in either acute or chronic nicotine-treated UAs. eNOS immunoreactivity was only detected in the endothelium of UAs, and eNOS protein levels were significantly decreased in UAs after chronic nicotine treatment. The results indicate impaired uterine vascular function by nicotine, which may lead to an increase in vascular resistance and a decrease in uterine blood flow. (Supported in part by TRDRP Award # 14FT-0075)
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