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Estrogen vasodilation

Kishnankutty S, Chiu T Mullen W, et al. Mechanisms of estrogen-induced vasodilation in vivo studies in canine coronary conductance and resistance arteries. J Am Coll Cardiol 1995 26 807-814. [Pg.353]

Estrogens have also been found to have direct effects on blood vessels, including increased synthesis of nitric oxide and increased vasodilation (Farhat et al., 1996 McCrohon et al., 1996). The observed decrease in the risk of cardiovascular disease and atherosclerosis by estrogens (Pines et al, 1997 Punnonen et al., 1995 Stampfer and Colditz, 1991) is thought to be due to the combined effects of estrogens on serum lipids and vascular reactivity. [Pg.299]

The mean uses per compound in Table V is 1.7. The mean uses per compound can be counted tor each ot the uses, it was shown (9) that mean uses per compound is distributed statistically and the outliers on each side could be identified. The ones with low mean uses per compound were highly specific uses such as antimicrobial, antineoplastics, antihistaminics, estrogenics, etc. The ones with high mean uses were the ones which were present in dominant use pairs or clusters such as diuretics, vasodilator, CNS depressant, etc., or which had old imprecise use descriptors such as sudorific, diaphoretic, dermatoses, etc. [Pg.102]

Rahimian R,Van BreemenC, Karkan D, DubeG, Laherl Estrogen augments cyclopiazonic acid-mediated, endothelium-dependent vasodilation. Eur J Pharmacol 327 143-9,1997... [Pg.221]

In the last decade, an expectation of coronary benefit had been a major reason for postmenopausal hormone use because observational studies indicated that women who use hormone therapy have a 35% to 50% lower risk of coronary heart disease than nonusers. In addition, previous studies have shown that estrogen exerts protective effects on the cardiovascular system, including lipid-lowering,antioxidant, and vasodilating effects. Nevertheless, recent randomized clinical trials have provided no evidence of cardiovascular disease protection and even some evidence of harm with hormone therapy " (Table 80-8). [Pg.1503]

Worboys S, Kotsopoulos D, Teede H, et al. Evidence that parenteral testosterone therapy may improve endothehum-dependent and -independent vasodilation in postmenopausal women already receiving estrogen. J Clin Endocrinol Metab 2001 86 158-161. [Pg.1511]

The use of selective ERa modulators has provided information similar to that obtained from ERKO transgenic mice. PPT stimulated uterine proliferation as well as ethinyl-estradiol, prevented bone mineral density loss in ovariectomized rats, lowered serum cholesterol levels and prevented hot flashes in a chemically induced hot flash rat model [17]. The use of PPTalso showed that ERa is primarily responsible for the effects of estrogen on the pituitary, vasodilation, neuroprotection, cardioprotec-tion and insulin sensitivity (reviewed in Ref. [18]). Protective effects were also... [Pg.50]

The incidence of cardiovascular disease is low in premenopausal women, rising rapidly after menopause, and epidemiological studies consistently showed an association between estrogen use and reduced cardiovascular disease in postmenopausal women. Furthermore, estrogens produce a favorable lipoprotein profile, promote vasodilation, inhibit the response to vascular injury, and reduce atherosclerosis. Studies such as these led to the widespread use of estrogen for prevention of cardiovascular disease in postmenopausal women. [Pg.249]


See other pages where Estrogen vasodilation is mentioned: [Pg.223]    [Pg.228]    [Pg.8]    [Pg.608]    [Pg.325]    [Pg.328]    [Pg.325]    [Pg.328]    [Pg.347]    [Pg.250]    [Pg.164]    [Pg.221]    [Pg.347]    [Pg.446]    [Pg.72]    [Pg.264]    [Pg.476]    [Pg.407]    [Pg.998]    [Pg.175]    [Pg.325]    [Pg.328]    [Pg.353]    [Pg.275]    [Pg.1812]    [Pg.1879]    [Pg.63]    [Pg.271]   
See also in sourсe #XX -- [ Pg.214 ]




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