Acute effect of 17 beta-estradiol on rabbit coronary artery contractile responses to endothelin-1

Jiang, Canwen; Sarrel, Philip M.; Poole-Wilson, P. A.; Collins, Peter

doi:10.1152/ajpheart.1992.263.1.h271

Cited by 115 publications

(103 citation statements)

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“…Second, oestrogen could act as an antioxidant [27] and thereby attenuate the degradation of NO by oxygen free radicals. Oestrogens could also modulate the vasoactive action of other endothelium-derived factors, such as prostacyclin and endothelin [28,29].…”

Section: Discussionmentioning

confidence: 99%

Effects of age, gender and metabolic factors on endothelium‐dependent vasodilation: a population‐based study

Sarabi

Millgård

Lind

1999

Journal of Internal Medicine

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Abstract. Sarabi M, Millga Êrd J, Lind L (University Hospital, Uppsala, Sweden). Effects of age, gender and metabolic factors on endothelium-dependent vasodilation: a population-based study. J Intern Med 1999; 246: 265±274.Objectives. A progressive decline in endotheliumdependent vasodilation (EDV) in the human forearm with age has previously been reported. The aim of this study was to evaluate the interplay between age, gender and metabolic factors on EDV in healthy subjects in a population-based study. Setting. Tertiary university hospital. Subjects and design. Thirty-six healthy men and 30 women, aged 20±69 years, underwent measurements of forearm blood flow (FBF) at rest and during local infusions of 2 and 4 mg min 21 of metacholine (evaluating EDV) and 5 and 10 mg min 21 of sodium nitroprusside (evaluating endothelium-independent vasodilation, EIDV) and during reactive hyperaemia by venous occlusion plethysmography. Results. Age was inversely related to EDV (r = ± 0.41, P , 0.05 in men; r = ± 0.61, P , 0.01 in women) and maximal FBF during reactive hyperaemia in both men and women. EIDV was significantly related to age in an inverse way in women only. EDV was more pronounced in females than in males before menopause (48 6 3 SD years, 635 6 186 vs. 502 6 269% in males, P , 0.05), but similar in women and men thereafter (374 6 141 vs. 370 6 185% in men). The slope of the regression line for the relationship between age and EDV was flatter in premenopausal than in postmenopausal women (± 2.3 vs. ± 6.4), whilst this slope was similar in younger and older men (± 5.5 vs. ± 5.3). In multiple regression analysis, fasting blood glucose levels and the waist/hip ratio remained the only significant predictors of EDV in men (P , 0.01 for both), whilst age was the only significant independent predictor of EDV in women (P , 0.01). Conclusion. The interplay between age and metabolic factors as determinants of endothelial function is different in healthy men and women.

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Section: Discussionmentioning

confidence: 99%

Effects of age, gender and metabolic factors on endothelium‐dependent vasodilation: a population‐based study

Sarabi

Millgård

Lind

1999

Journal of Internal Medicine

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“…Studies have documented that E2 can induce relaxation of coronary arteries, reverse acetylcholine-induced vasoconstriction and improve exercise-induced myocardial ischemia in women with coronary artery disease (29)(30)(31)(32). Collins et al (33) showed that E2 decreases acetylcholine-induced coronary artery responses only in women, but not in men.…”

Section: Estrogen and Vascular Tonementioning

confidence: 99%

Estrogen replacement therapy and cardioprotection: mechanisms and controversies

Subbiah

2002

Braz J Med Biol Res

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Epidemiological and case-controlled studies suggest that estrogen replacement therapy might be beneficial in terms of primary prevention of coronary heart disease (CHD). This beneficial effect of estrogens was initially considered to be due to the reduction of low density lipoproteins (LDL) and to increases in high density lipoproteins (HDL). Recent studies have shown that estrogens protect against oxidative stress and decrease LDL oxidation. Estrogens have direct effects on the arterial tissue and modulate vascular reactivity through nitric oxide and prostaglandin synthesis. While many of the effects of estrogen on vascular tissue are believed to be mediated by estrogen receptors a and ß, there is evidence for immediate non-genomic effects. The role of HDL in interacting with 17ß-estradiol including its esterification and transfer of esterified estrogens to LDL is beginning to be elucidated. Despite the suggested positive effects of estrogens, two recent placebo-controlled clinical trials in women with CHD did not detect any beneficial effects on overall coronary events with estrogen therapy. In fact, there was an increase in CHD events in some women. Mutations in thrombogenic genes (factor V Leiden, prothrombin mutation, etc.) in a subset of women may play a role in this unexpected finding. Thus, the cardioprotective effect of estrogens appears to be more complicated than originally thought and requires more research.

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“…However, systemic effects of estrogens do not account fo ~" the majority of the observed atheroprotective effects of E2 [2.3,15,16]. In an effort to reveal additional pathways that may mediate the atheroprotective effects of E2, direct effects of E2 ol ~, vascular cells are currently being investigated (reviewed in [1 '] Direct effects of E2 on vascular cell function were first suggested decades ago [7,18] and have since been shown both in whole animal and in vitro studies [10,[19][20][21][22][23][24][25][26][27][28][29][30]. However, the signaling pathways involved in the direct effects of E2 on vascular cells are not yet characterized.…”

Section: Introductionmentioning

confidence: 99%