Menopausal Oestrogen Therapy and Protection From Death From Ischaemic Heart Disease

Ross, R. K.; Mack, ThomasM.; Paganini‐Hill, Annlia; Arthur, Mary E.; Henderson, B. E.

doi:10.1016/s0140-6736(81)92138-3

Cited by 334 publications

(65 citation statements)

References 11 publications

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“…Other studies have indicated that oral oestrogen replacement treatment may reduce risk (Bain et al, 1981;Ross et al, 1981). Unfortunately, as yet no prospective data on the long-term use of tamoxifen and cardiovascular risk have been published, or are likely to be available in the nearest future.…”

Section: Methodsmentioning

confidence: 99%

Tamoxifen, serum lipoproteins and cardiovascular risk

Bruning

Bonfrèr²,

Hart³

et al. 1988

Br J Cancer

138

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Summary The influence of tamoxifen on plasma lipids and lipoproteins was monitored in 46 postmenopausal and 8 premenopausal women treated for advanced breast cancer up till 6 months. Total cholesterol (total-C) did not significantly change. However, high density lipoprotein cholesterol (HDL-C) and the HDL-C/ total-C ratio rose significantly. Low density lipoprotein cholesterol was significantly decreased. Triglycerides and free fatty acids did not change markedly. The concomitant rise of sex hormone binding globulin and thyroxine binding globulin indicates that the increase of HDL-C with prolonged use of tamoxifen is compatible with an intrinsic oestrogenic effect of tamoxifen on the liver. The increased HDL-C/total-C ratio lends no support to the concern that long-term administration of this anti-oestrogenic drug might lead to an increased cardiovascular risk.

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Section: Methodsmentioning

confidence: 99%

Tamoxifen, serum lipoproteins and cardiovascular risk

Bruning

Bonfrèr²,

Hart³

et al. 1988

Br J Cancer

138

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“…The following chemicals: [17a-methyl-3 H3]R1881 (methyltrlenolone, specific activity 87 Ci/mmol), [1,2,4,5,6,7,16, H8]5a-dihydrotestosterone (5a-DHT, specific activity 208 Ci/mmol), [11 B-methoxy-3 H3]R2858 (moxestrol, specific activity 79.2 Ci/mmol), [2,4,6,7,16,17-3 H 6 (A/)]estradiol (specific activity 134 Ci/mmol), [ 14 C(U)]uridine diphosphate glucose (UDPG, specific activity 343 mCi/mmol), and radioinert R1881 and R2858 were obtained from New England Nuclear Corporation, Boston, Massachusetts. These compounds were used as provided by the manufacturer.…”

Section: Chemicalsmentioning

confidence: 99%

Gender and baboon aortic steroid hormone receptors.

Lin¹,

González²,

Carey³

et al. 1987

Arteriosclerosis

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To examine the potential of steroid hormones to serve as putative regulators of aortic cell function, we defined hormone receptor content and distribution In intact baboons. Total androgen receptor content In baboon aortic arch, thoracic arch, and abdominal aorta of young mature males was Indistinguishable from that of proestrus females. However, 30% to 40% of male aortic androgen receptors were In the nuclear fraction, whereas all aortic androgen receptors of proestrus females were In the cytoplasmlc fraction. Cytoplasmlc fraction estrogen receptor content of aortic arch and thoracic aorta of Intact males was indistinguishable from that of proestrus females. However, cytoplasmlc fraction estrogen receptor content of abdominal aorta of proestrus females was significantly greater than that of males. Nuclear fraction estrogen receptors were not detectable In either male or proestrus female baboon aortas. To assess effects of endogenous estrogen on aortic progesterone receptor content, we quantified cytoplasmlc fraction progesterone receptors and found that content of proestrus female aortic arch was not significantly different from that of males. However, cytoplasmlc fraction progesterone receptor content of thoracic and abdominal aorta of proestrus females was significantly higher than that of males. To determine whether differences In aortic receptor content or distribution were associated with changes In aortic cell function, we quantified the activity of two enzymes of glycosamlnoglycan metabolism. Aortic B-glucuronldase activity was not different In male or proestrus female baboons. Urldlne dlphosphate glucose (UDPG) dehydrogenase activity of aortic arch and thoracic aorta of proestrus female baboons was not different from that of males; however, UDPG dehydrogenase activity of abdominal aorta of proestrus females was greater than that of males. Our studies establish endogenous androgen regulation of Intracellular distribution of baboon aortic androgen receptors and imply that these receptors are physiologically functional. The higher cytoplasmlc fraction progesterone receptor content of female thoracic and abdominal aorta, as compared to that of males, suggests aortic estrogen receptors also are physiologically functional. These findings establish that baboon aortic steroid hormone receptor content and distribution Is sexually dimorphic, as Is the case for rodents. However, the essential Identity of B-glucuronldase or UDPG dehydrogenase activity In male and female baboon aortas Indicates that baboon aortic glycosamlnoglycan metabolism Is not sexually dimorphic. The fact that aspects of aortic steroid hormone receptor homeostasls and steroid hormone regulation of aortic UDPG dehydrogenase and B-glucuronldase activity significantly differ In baboons and rodents Implies complex effects of steroid hormones which may be speciesspecific. (Arteriosclerosis 7:248-255, May/June 1987) I t is well established that men have a higher incidence of coronary heart disease (CHD) than age-matched females; however, the underlyi...

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“…[11 B-Methoxy-3 H3]R2858, moxestrol (specific activity 87 Ci/mmol), radioinert R2858, [2,4,6,7,16, H 6 (N)]estradiol (specific activity 134 Ci/mmol), radioinert R5020 (promegestone), and radioinert R1881 (methyltrienolone) were obtained from New England Nuclear Corporation, Boston, Massachusetts, and were used as provided by the manufacturer. Sources for other chemicals used in this study were previously described.…”

Section: Chemicalsmentioning

confidence: 99%

Estrogen-mediated cytoplasmic and nuclear distribution of rat cardiovascular estrogen receptors.

Lin

Shain

1985

Arteriosclerosis

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We used either the synthetic estrogen R2858 (moxestrol) or estradiol-17(3 to characterize estrogen receptors in cytoplasmic (R2858) and nuclear (estradiol-17B) preparations from rat aorta and myocardium. Relative steroid specificity studies showed that only estrogens were effective inhibitors of R2858 or estradiol-171) binding to aortic and myocardial estrogen receptors, whereas androgens, progestins, and cortisol were ineffective inhibitors. Low ionic strength sucrose density gradient analyses showed that myocardial estrogen receptors that localized in the cytoplasmic fraction migrated as macromolecules with sedimentation coefficients of 8S to 9S. In contrast, two binding components of sedimentation coefficients 8S to 9S and 10S to 11S were characteristic of the estrogen receptors localized in aortic cytoplasmic preparations. High ionic strength sucrose density gradient analysis showed that aortic and myocardial estrogen receptors localized in the nuclear fraction migrated as macromolecules with sedimentation coefficients of 4S to 6S. Saturation analyses showed that aortic and myocardial cytoplasmic preparations from intact young mature male rats contained 50.6 ± 12.9 (mean ± SD) and 51.0 ± 14.1 fmol receptor/mg DNA, respectively. The respective R2858 dissociation constants were 0.42 and 0.15 nM. Estrogen receptors could not be demonstrated in nuclear preparations from cardiovasculature of intact males. Estradiol-17(3 injection of intact young mature male rats caused "depletion" of aortic and myocardial cytoplasmic fraction estrogen receptors and resulted in the appearance of 51.9 ± 21.0 and 36.9 ± 9.5 fmol receptor/mg DNA in the corresponding nuclear fractions. The respective estradiol-17(3 dissociation constants were 1.56 and 0.71 nM. Increased estrogen receptor content of cardiovascular nuclear fractions of estradiol-17(3 injected male rats correlated well with the concomitant decreased cytoplasmic fraction receptor content. The ability of estradiol-17(3 to affect localization of cardiovascular estrogen receptors between cytoplasmic and nuclear fractions suggests these estrogen receptors are physiologically functional and indicates that estrogen may directly regulate cardiovascular cell function. (Arteriosclerosis 5:668-677, November/December 1985)T he higher incidence of coronary heart disease (CHD) in postmenopausal women as compared to premenopausal individuals 12 and in oral contraceptive users as compared to nonusers 23 and the decreased mortality of estrogen-only users as compared to nonusers 2 -"• 5 has suggested a possible Received December 17,1984; revision accepted July 10,1985. etiologic role for estrogens in CHD. This impression is supported by reports of higher plasma estrogen content in males who survived a myocardial infarction 6 " 11 or have documented coronary artery occlusion in the absence of an infarction. 8 ' 9 These clinical observations have led some investigators to conclude that hyperestrogenemia is an additional risk factor for CHD in males. 6810

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Menopausal Oestrogen Therapy and Protection From Death From Ischaemic Heart Disease

Cited by 334 publications

References 11 publications

Tamoxifen, serum lipoproteins and cardiovascular risk

Tamoxifen, serum lipoproteins and cardiovascular risk

Gender and baboon aortic steroid hormone receptors.

Estrogen-mediated cytoplasmic and nuclear distribution of rat cardiovascular estrogen receptors.

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