Regulation of prostacyclin and thromboxane production by human umbilical vessels: The effect of estradiol and progesterone in a superfusion model

Mäkilä, U.-M.; Wahlberg, L.; Viinikka, Lasse; Ylikorkala, Olavi

doi:10.1016/s0262-1746(82)80003-6

Cited by 72 publications

(2 citation statements)

References 26 publications

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“…The dose of MPA administered by Sullivan et al 52 was double that used in other studies, 49 in which no effect on peripheral blood flow of the added progestin was noted. Estrogen has also been reported to stimulate endothelial production of prostacyclin, 56 a potent vasodilator as well as an inhibitor of platelet aggregation.…”

Section: Vascular Effectsmentioning

confidence: 99%

The Role of Hormone Replacement Therapy in the Prevention of Postmenopausal Heart Disease

Mosca¹

2000

Arch Intern Med

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Coronary heart disease is the single leading cause of death in women and a significant cause of disability. Menopause adversely affects several risk factors for coronary heart disease, suggesting that hormones influence the risk of coronary heart disease in postmenopausal women. This article reviews the observational and clinical trial data evaluating the relation between cardiovascular disease and hormone replacement therapy. Biological mechanisms of estrogen and the impact of adding progestins are emphasized. Potential risks and benefits of therapy are discussed. The relative effects of other estrogen and lipid-lowering therapies for preventing coronary heart disease in postmenopausal women are highlighted.

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Section: Vascular Effectsmentioning

confidence: 99%

The Role of Hormone Replacement Therapy in the Prevention of Postmenopausal Heart Disease

Mosca¹

2000

Arch Intern Med

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“…Sex hormones have been found to affect a number of pathways in PG formation. For example, estrogens have been shown to increase prostacyclin formation in human umbilical vessels (39,40), and cyclooxygenase and prostacyclin synthase activities in rat aortic smooth-muscle cells (41). In contrast, estrogens have little effect on thromboxane synthesis (40) or result in decreased thromboxane formation (42).…”

Section: Discussionmentioning

confidence: 99%

Insulin Sensitivity and Cardiovascular Risk Factors in Ovariectomized Monkeys with Estradiol Alone or Combined with Nomegestrol Acetate¹

Wagner

Thomas²,

Williams³

et al. 1998

The Journal of Clinical Endocrinology & Metabolism

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We have previously shown that medroxyprogesterone acetate (MPA), either alone or combined with conjugated equine estrogens (CEE), significantly decreased insulin sensitivity (SI), compared with both untreated controls and those treated with CEE alone. The purpose of this study was to determine the effects of estradiol (E2), with and without nomegestrol acetate (NA; a potent progestin that lacks androgenic activity), on SI and arterial antioxidant activity, as determined by F2-isoprostanes. Thirty-six adult female cynomolgus monkeys (Macaca fascicularis) were ovariectomized and fed a moderately atherogenic diet, with one of the following three treatments added to the diet, for 12 weeks: 1) no treatment (control); 2) E2; or 3) continuous combined E2 + NA (E2+NA). SI and glucose effectiveness were assessed by the frequently sampled i.v. glucose tolerance test using a third-phase insulin infusion after 10 weeks of treatment. Cholesterol content and F2-isoprostanes were measured in the thoracic aorta after 12 weeks of treatment. E2 treatment resulted in a significantly greater SI, compared with control or E2+NA-treated monkeys (10.03 +/- 0.91 vs. 6.35 and 6.49 x 10(-4) min(-1) microU(-1) mL; P < 0.05). In contrast to our studies of CEE and MPA, E2+NA treatment, though reducing the SI below that of the E2 group, did not reduce the SI below that of control monkeys. As expected, the short period of treatment resulted in no significant differences in aortic cholesterol content. There was no treatment effect on total F2-isoprostanes (representing F2-isoprostane formation caused primarily by autooxidation), suggesting minimal antioxidant activity. However, there was a treatment difference in the prostaglandin F2alpha (PGF2alpha) isomer (a prostaglandin (PG) isomer formed by both autooxidation of arachidonate and cyclooxygenase activity). PGF2alpha concentrations were 32% lower with E2 treatment, compared with controls, and 36% lower, compared with E2+NA treatment (0.48 +/- 0.08 vs. 0.71 +/- 0.12 and 0.75 +/- 0.06; P < 0.05), suggesting differences in PG synthesis between hormone treatments. In conclusion, NA, a progestin without androgenic activity, may still affect some cardiovascular risk factors differently than estrogen-only therapy. However, it seems to be less detrimental than MPA.

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Decreased Risk of Stroke Among Postmenopausal Hormone Users

Finucane

Madans²,

Bush³

et al. 1993

Arch Intern Med

186

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Regulation of prostacyclin and thromboxane production by human umbilical vessels: The effect of estradiol and progesterone in a superfusion model

Cited by 72 publications

References 26 publications

The Role of Hormone Replacement Therapy in the Prevention of Postmenopausal Heart Disease

The Role of Hormone Replacement Therapy in the Prevention of Postmenopausal Heart Disease

Insulin Sensitivity and Cardiovascular Risk Factors in Ovariectomized Monkeys with Estradiol Alone or Combined with Nomegestrol Acetate¹

Decreased Risk of Stroke Among Postmenopausal Hormone Users

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Regulation of prostacyclin and thromboxane production by human umbilical vessels: The effect of estradiol and progesterone in a superfusion model

Cited by 72 publications

References 26 publications

The Role of Hormone Replacement Therapy in the Prevention of Postmenopausal Heart Disease

The Role of Hormone Replacement Therapy in the Prevention of Postmenopausal Heart Disease

Insulin Sensitivity and Cardiovascular Risk Factors in Ovariectomized Monkeys with Estradiol Alone or Combined with Nomegestrol Acetate1

Decreased Risk of Stroke Among Postmenopausal Hormone Users

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Insulin Sensitivity and Cardiovascular Risk Factors in Ovariectomized Monkeys with Estradiol Alone or Combined with Nomegestrol Acetate¹