Thrombosis and atherosclerosis prevention by estrogens in hyperlipemic rats

Renaud, S.

doi:10.1016/0021-9150(70)90050-x

Cited by 11 publications

(4 citation statements)

References 20 publications

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“…Estradiol treatment also inhibited myointimal thickening in rabbit abdominal aorta and iliac artery subjected to balloon injury (68). The development of medial thickening in rat distal pulmonary arteries exposed to chronic hypoxia (69) or injected with the toxic Estrogen also protects against the development of dietinduced atherosclerosis in rats (71) and rabbits (72,73). The anti-atherogenic effect of estrogen in these studies was attributed to a direct effect of the hormone on HDL cholesterol level.…”

Section: Estrogen and Vascular Smooth Muscle Cell Proliferationmentioning

confidence: 92%

The vascular protective effects of estrogen

1996

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There is now strong epidemiological evidence that estrogen replacement therapy has a protective effect in postmenopausal women. The cardiovascular protective action of estrogen is reported to be mediated indirectly by an effect on lipoprotein metabolism and by a direct effect on the vessel wall itself. Estrogen is active both in vascular smooth muscle and endothelium. Functionally competent estrogen receptors have been identified in vascular smooth muscle cells, and specific binding sites have been demonstrated in endothelium. Estrogen administration promotes vasodilation both in human and experimental animals, in part by stimulating] prostacyclin and nitric oxide synthesis. Both the prostaglandin synthase and the constitutive nitric oxide synthase were recently reported to be induced by estrogen treatment. In vitro, estrogen exerts a direct inhibitory effect on the smooth muscle by inhibiting calcium influx. In addition, estrogen inhibits vascular smooth muscle cell proliferation. In vivo, estradiol-17 beta prevents neointimal thickening after balloon injury and in rabbit cardiac transplant allografts. These data are consistent with in vitro studies wherein estrogen inhibits [3H]thymidine uptake by arterial segments from porcine coronary artery as well as proliferation of rabbit aortic vascular smooth muscle cells induced by hyperlipedemic serum. Recent studies have also reported an effect of estrogen on directed vascular smooth muscle cell migration. Furthermore, like other steroids, the effect of estrogen on the vessel wall has a rapid nongenomic component involving membrane phenomena, such as alteration of membrane ionic permeability and activation of membrane-bound enzymes, as well as the classical genomic effect involving estrogen receptor activation and gene expression. The nature of these estrogen response genes in the vessel wall and their relation to vasodilation and antiproliferation remain to be determined.

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Section: Estrogen and Vascular Smooth Muscle Cell Proliferationmentioning

confidence: 92%

The vascular protective effects of estrogen

1996

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“…Oestradiol also inhibits experimentally induced atherosclerosis in rat and rabbit (Moskowitz et al, 1956;Renaud et al, 1970), as well as myointimal proliferation in aorta and cardiac allograft associated with abdominal aorta transection and surgical re-anastomosis in the rabbit (Foegh et al, 1987;Cheng et al, 1991). Studies in the pulmonary circulation however, suggest a facilitating role of oestrogen on the development of pulmonary vascular wall hypertrophy associated with pulmonary hypertension.…”

Section: Effect Of Tamoxifenmentioning

confidence: 99%

“…Clinically, oestrogen replacement therapy is associated with decreased incidence of coronary heart disease (Stampfer et al, 1991). Oestradiol-17,B also protects against the development of experimental atherosclerosis (Renaud, 1970;Foegh et al, 1987;Clarkson et al, 1990). The effect of oestrogen on pulmonary vascular smooth muscle cell (VSMC) growth and proliferation has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

In vitro effect of oestradiol on thymidine uptake in pulmonary vascular smooth muscle cell: role of the endothelium

Farhat

Vargas

Dingaan

et al. 1992

British J Pharmacology

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1 The effect of different concentrations of oestradiol-171P (3-300 nM) on [3H]-thymidine uptake was studied in segments from canine pulmonary artery, and cultures of rat pulmonary vascular smooth muscle cells (VSMC).2 Incubation with oestradiol-1 7P for 24 h, potentiated in a concentration-dependent manner [3H]-thymidine uptake in VSMC cultures. 3 Oestradiol-1 71B potentiated thymidine uptake by pulmonary arterial segments but only when the endothelium had been removed. Autoradiography showed dense incorporation of radioactive thymidine in the vascular smooth muscle cells of the media. 4 The non-steroidal oestrogen, stilboestrol (300 nM), also significantly potentiated [3H]-thymidine uptake, in both VSMC cultures and pulmonary artery segments. Testosterone was ineffective at a similar concentration.5 Pre-incubation of the pulmonary VSMC with the anti-oestrogen tamoxifen (I ylM) antagonized the potentiating effect of oestradiol-171P on [3H]-thymidine incorporation. The effect of tamoxifen was less pronounced in pulmonary arterial segments. 6 These data suggest that oestrogen may promote proliferation of pulmonary VSMC. Endothelial injury or dysfunction may be an important factor in the expression of the oestrogenic effect. 7 We speculate that plasma oestrogen may be a contributing factor to the proliferative lesion observed in certain forms of pulmonary vascular injury in women.

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“…Oestradiol also inhibits diet-induced atherosclerosis in rat and rabbit (Moskowitz et al, 1956;Constantinides et al, 1962;Renaud, 1970). Ethinyl oestradiol has been reported to reduce plaque area in the aorta of cholesterol-fed female Macaca fascicularis (Clarkson et al, 1987;.…”

Section: Introductionmentioning

confidence: 99%

Oestradiol inhibits smooth muscle cell proliferation of pig coronary artery

Vargas

Wróblewska

Rego

et al. 1993

British J Pharmacology

164

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1 The effect of oestradiol 17p on vascular smooth muscle proliferation was examined in segments of the pig left anterior descending coronary artery (LAD). It was established by cytochemical techniques that out-growth from the segments was composed of vascular smooth muscle cells. 2 [3H]-thymidine uptake by pig LAD segments was used as an index of vascular smooth muscle cell proliferation. Nitroprusside and forskolin significantly inhibited [3H]-thymidine uptake and were used as positive controls. 3 Oestradiol 171 (180 -360 nM) inhibited thymidine uptake by pig LAD segments (P <0.05). The inhibition was observed only in the absence of phenol red, which is a weak oestrogen receptor agonist. The anti-oestrogens tamoxifen and its more potent metabolite 4-hydroxytamoxifen, both of which are partial oestrogen receptor agonists, also significantly inhibited thymidine uptake. However, pretreatment with either tamoxifen or 4-hydroxytamoxifen did not signficantly block oestradiol 17p-induced inhibition of thymidine uptake. 5 The data suggest that oestradiol 171 inhibits smooth muscle cell proliferation in porcine LAD segments, possibly through an oestrogen receptor mechanism. This in vitro effect suggests an in vivo role for oestradiol 171 in directly protecting coronary arteries against myointimal proliferation in premenopausal women.

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Thrombosis and atherosclerosis prevention by estrogens in hyperlipemic rats

Cited by 11 publications

References 20 publications

The vascular protective effects of estrogen

The vascular protective effects of estrogen

In vitro effect of oestradiol on thymidine uptake in pulmonary vascular smooth muscle cell: role of the endothelium

Oestradiol inhibits smooth muscle cell proliferation of pig coronary artery

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