{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:53:02Z","timestamp":1787017982120,"version":"build-2736575974"},"reference-count":32,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["ATVB"],"published-print":{"date-parts":[[1999,4]]},"abstract":"<jats:p>\n                    <jats:italic>Abstract<\/jats:italic>\n                    \u2014The clinical observation that coronary artery disease is more common in men and postmenopausal women than in premenopausal women has suggested cardioprotective effects of female sex hormones including hormone-mediated coronary vasodilation. The purpose of this study was to investigate whether the sex hormone-induced coronary relaxation is caused by inhibition of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    mobilization into coronary smooth muscle. The effects of 17\u03b2-estradiol, progesterone, and testosterone on vascular reactivity and\n                    <jats:sup>45<\/jats:sup>\n                    Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx were tested in deendothelialized coronary artery strips isolated from castrated male pigs. Prostaglandin F\n                    <jats:sub>2\u03b1<\/jats:sub>\n                    (PGF\n                    <jats:sub>2\u03b1<\/jats:sub>\n                    ) (10\n                    <jats:sup>\u22125<\/jats:sup>\n                    mol\/L) caused significant, maintained contraction of coronary artery strips. Caffeine (25 mmol\/L), an activator of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release from intracellular stores, caused transient contraction in Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -free solution whereas membrane depolarization by 96 mmol\/L KCl, an activator of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry, caused maintained contraction in the presence of external Ca\n                    <jats:sup>2+<\/jats:sup>\n                    . The 3 sex hormones caused significant and concentration-dependent relaxation of PGF\n                    <jats:sub>2\u03b1<\/jats:sub>\n                    - and 96 mmol\/L KCl-induced contractions with 17\u03b2-estradiol being the most effective. The sex hormones did not significantly affect the transient caffeine contraction in Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -free solution. In contrast, the sex hormones significantly inhibited the PGF\n                    <jats:sub>2\u03b1<\/jats:sub>\n                    - and KCl-induced\n                    <jats:sup>45<\/jats:sup>\n                    Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx. 17\u03b2-Estradiol caused similar inhibition of PGF\n                    <jats:sub>2\u03b1<\/jats:sub>\n                    - and KCl-induced contractions, suggesting inhibition of the same Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry mechanism. However, progesterone and testosterone caused greater relaxation of PGF\n                    <jats:sub>2\u03b1<\/jats:sub>\n                    -induced contraction than of KCl-induced contraction. We conclude that in coronary arteries of castrated male pigs, sex hormones inhibit Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry from extracellular space but not Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release from intracellular stores. 17\u03b2-Estradiol mainly inhibits Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry, whereas progesterone and testosterone cause coronary relaxation by inhibiting other mechanisms in addition to Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry.\n                  <\/jats:p>","DOI":"10.1161\/01.atv.19.4.1034","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T15:44:19Z","timestamp":1308325459000},"page":"1034-1040","source":"Crossref","is-referenced-by-count":129,"title":["Antagonistic Effects of 17\u03b2-Estradiol, Progesterone, and Testosterone on Ca\n                    <sup>2+<\/sup>\n                    Entry Mechanisms of Coronary Vasoconstriction"],"prefix":"10.1161","volume":"19","author":[{"given":"Janice K.","family":"Crews","sequence":"first","affiliation":[{"name":"From the Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raouf A.","family":"Khalil","sequence":"additional","affiliation":[{"name":"From the Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199201233260406"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199110243251702"},{"key":"e_1_3_2_3_2","first-page":"1","volume":"12","year":"1983","journal-title":"Artery"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1991.03460140089033"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.92.1.5"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0735-1097(92)90117-6"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0735-1097(92)90116-5"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/0031-9384(89)90086-3"},{"key":"e_1_3_2_9_2","first-page":"E536","volume":"256","year":"1989","journal-title":". 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