Ethinyl estradiol acutely attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women.

Reis, Steven E.; Gloth, Sean T.; Blumenthal, Roger S.; Resar, Jon R.; Zacur, Howard A.; Gerstenblith, Gary; Brinker, Jeffrey A.

doi:10.1161/01.cir.89.1.52

Cited by 504 publications

(198 citation statements)

References 46 publications

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“…In both women and female experimental animals, ovariectomy caused a deterioration in EDV, whilst oestrogen replacement restored EDV [21,22]. In humans, acute administration of oestrogen improves vasodilatation induced by acetylcholine in coronary arteries [23,24]. The assumption that this improvement in EDV is mediated by the NO system is further strengthened by the finding that oestrogen supplementation increased the levels of nitrate and nitrite, the breakdown products of NO, in postmenopausal women [25].…”

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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“…Furthermore, a maintained nocturnal dipping phenomenon was still apparent during oestrogen treatment. It is believed that oestrogen acts as a vasodilator via several different mechanisms, eg, directly via endothelium-dependent and -independent mechanims, 18,19 via calcium-channel blocking-like effects 20 and via interaction with the renin-angiotensin system. 21 Oestrogen also elicits an effect on prostacyclin production which also has a vasodilating potential.…”

Section: Discussionmentioning

confidence: 99%

Transdermal oestrogen reduces daytime blood pressure in hypertensive women

et al. 1998

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The aim of this study was to investigate the acute effects of transdermally administered 17-␤-oestradiol on ambulatory blood pressure (BP) in hypertensive, postmenopausal women. Thirteen postmenopausal women with ongoing treatment for hypertension were included in this placebo-controlled, double-blind cross-over study. Ambulatory recordings of BP and heart rate were performed during 24 h on two occasions, separated by at least 1 week, after application of a patch containing either 100 g per 24 h 17-␤-oestradiol or placebo. Serum oestradiol was increased (PϽ0.001) during active treatment (139.2 ± 21.1 pg/ml) compared with the baseline postmenopausal levels recorded during placebo (40.5 ± 2.2 pg/ml). No rise in BP was found in office BP

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“…Estrogen is generally considered to be cardioprotective in coronary heart disease, by mechanism(s) yet to be elucidated. Recent findings indicate that acute exogenous estrogen increases coronary flow and partially restores coronary va soreactivity to vasodilators (Reis et al , 1994).…”

Section: Discussionmentioning

confidence: 99%

Postischemic Cerebral Blood Flow Recovery in the Female: Effect of 17β-Estradiol

Hurn

Littleton-Kearney

Kirsch

et al. 1995

J Cereb Blood Flow Metab

147

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Summary: Female reproductive hormones are consid ered to be protective agents in atherosclerotic vascular disease and stroke. The present study determined if there are unique cerebrovascular responses in female animals to global cerebral ischemia and if 17J3-estradiol is impor tant to postischemic outcome in brain. Three groups of anesthetized, sexually mature rabbits were treated with normotensive four-vessel occlusion (6 min) and 3 h of reperfusion: females chronically instrumented with 1713-estradiol implants (EFEM; n = 8, plasma estradiol level = 365 ± 48 pg/ml), untreated females (FEM; n = 8, estradiol = 13 ± 3 pg/ml), and untreated males (M; n = 8, estradiol < limit of radioimmunoassay). CBF (micro spheres) and somatosensory evoked potential (SEP) am plitude were measured during ischemia/reperfusion. Baseline hemispheric blood flow and regional flow distri-The incidence of atherosclerotic vascular disease in premenopausal women is less than in men, but this difference disappears after menopause (Bush and Miller, 1987; Wolf et aI., 1987; Barrett-Connor and Bush, 199 1; Sivenius et aI. , 199 1). These obser vations have historically been interpreted as evi dence that female reproductive hormones confer vascular protection in ischemic heart disease and stroke. However, it is unclear if estrogen per se is critical to stroke risk or by what mechanism protec tion is achieved. Further, the presence of vascular responses unique to the female in an ongoing cere- 666bution were not altered by chronic estradiol treatment. Hemispheric blood flow was equivalently reduced during ischemia in FEM and M (6 ± 1 and 9 ± 2 ml min -I 100 g-I, respectively); however postischemic hyperemia was greater in FEM than M (CBF = 25 7 ± 27 and 18 3 ± 27 ml min -1 100 g -I. However, EFEM experienced higher CBF during ischemia (e.g., 13 ± 2ml min-1100 g-l) and less hyperemia (134 ± 4 ml min -I 100 g-I in hemi spheres) in numerous brain regions than FEM. CBF at 3 h reperfusion was not different among the groups. Recov ery of SEPs was incomplete and similar in all groups. We conclude that chronic exogenous 17J3-estradiol treatment increases CBF during global incomplete ischemia and ameliorates postischemic hyperemia in the female animal.

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Ethinyl estradiol acutely attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women.

Cited by 504 publications

References 46 publications

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

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

Transdermal oestrogen reduces daytime blood pressure in hypertensive women

Postischemic Cerebral Blood Flow Recovery in the Female: Effect of 17β-Estradiol

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