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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is widely accepted that in women, estrogens provide protection against the development of cardiovascular disease. However, the cardiovascular role of estrogens in men remains uncertain, despite preliminary evidence that endogenous estrogens produced by aromatization of androgenic precursors are of physiological importance. Hypogonadal men have very low levels of circulating estrogen. We studied the responsiveness of forearm resistance arteries to vasoconstrictor and vasodilator agents in 12 men (mean+/-SEM age, 68.7+/-2.6 years) rendered hypogonadal as a result of treatment for prostatic cancer, before and after 8 weeks of estrogen supplementation (estradiol valerate 1 mg daily; n=7) or placebo (n=5). Forearm blood flow was measured by venous occlusion plethysmography, and vasoactive agents were infused through a brachial artery cannula in doses that did not affect blood pressure or heart rate. Estrogen supplementation was well tolerated, with no adverse effects. After estrogen treatment, mean estradiol levels increased from <30 to 308+/-65 pmol/L, and both systolic and diastolic blood pressures were reduced. HDL cholesterol levels increased significantly, and vasoconstrictor responses to the NO synthase inhibitor N(G)-monomethyl-L-arginine (1, 2, 4 micromol/min) were enhanced. Vasoconstrictor responses to angiotensin II (8, 16, 32 ng/min) were markedly attenuated by estrogen treatment, as were vasoconstrictor responses to norepinephrine (25, 50, 100 ng/min). Estrogen did not alter the vasodilator responses to acetylcholine (9.25, 18.5, 37 microgram/min) or to the endothelium-independent agent sodium nitroprusside (1.6 microgram/min). Responses to all vasoactive agents were unchanged after administration of placebo. We conclude that low-dose estrogen supplementation in hypogonadal men is well tolerated, lowers blood pressure, and may affect vascular reactivity in a manner that is potentially beneficial, through several mechanisms, including enhancement of basal NO release and attenuation of vasoconstrictor responses to angiotensin II and norepinephrine. These findings suggest the need to consider a possible clinical role for estrogenic compounds in cardiovascular risk reduction in some groups of men.
Hypertension 2001 Nov
PMID:Low-dose estrogen supplementation improves vascular function in hypogonadal men. 1171 90

Hypertension, central obesity and dyslipidemia are associated with high cardiovascular risk. Estrogen therapy in women has beneficial effects on some of these metabolic cardiovascular risk factors. It is not known whether dietary estrogens have similar effects, especially in Western populations. We studied the association between dietary phytoestrogen intake and metabolic cardiovascular risk factors in postmenopausal women. For this purpose, 939 postmenopausal women participating in the Framingham Offspring Study were included in this cross-sectional study. Mean blood pressure, waist-hip ratio (WHR) and lipoprotein levels were determined in quartile categories of dietary phytoestrogen (isoflavones and lignans) intake, determined by a food-frequency questionnaire. In addition, a metabolic syndrome score was defined according to WHO criteria (range 0-6). The WHR was lower in women in the highest quartile of intake of lignans compared with the lowest [-0.017; 95% confidence interval (CI) -0.030 to -0.0016]. In the highest quartile of intake of isoflavones, plasma triglyceride levels were 0.16 mmol/L lower (95% CI, -0.30 to -0.02) compared with the lowest quartile of isoflavones; for lignan intake, this difference was 0.23 mmol/L (95% CI, -0.37 to -0.09). In the highest quartile of isoflavone intake, the mean cardiovascular risk factor metabolic score was 0.43 points lower (95% CI, -0.70 to -0.16) than the lowest quartile. The difference in this score between the extreme quartiles of intake of lignans was -0.55 points (95% CI, -0.82 to -0.28). In conclusion, high intake of phytoestrogens in postmenopausal women appears to be associated with a favorable metabolic cardiovascular risk profile.
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PMID:Dietary intake of phytoestrogens is associated with a favorable metabolic cardiovascular risk profile in postmenopausal U.S.women: the Framingham study. 1182 90

Estrogen receptors (ESR) 1 and 2 are expressed in the normal and atherosclerotic arteries mediating the atheroprotective action of estrogen to artery wall cells. Whether variants of these receptor genes associate with autopsy-verified coronary artery wall atherosclerosis is not known. This study investigated whether variants of the ESR1 gene are associated with autopsy-verified coronary artery wall atherosclerosis and thrombosis. Coronary arteries were taken from 300 white Finnish male autopsy cases aged 33-69 years included in the Helsinki Sudden Death Study. Areas of coronary wall covered with fatty streaks, fibrotic, calcified, and complicated lesions were measured using computer-assisted planimetry and related to ESR1 PvuII genotypes (P/P, P/p, and p/p) determined by PCR. The mean area of complicated lesions of three major coronaries and the presence of coronary thrombosis were significantly associated with the ESR1 genotype in men aged 53 years or older (median age as a cut off point). No such association was found in men aged under 53 years. After adjusting for age and body mass index the men aged 53 years or over with P/p and P/P genotype had areas of complicated lesions on average two- and fivefold larger than subjects with the p/p genotype. The age and body mass index adjusted odds ratios for coronary thrombosis were 6.2 for P/p and 10.6 for P/P compared to men with the p/p genotype. After additional adjustment for diabetes and hypertension the ESR1 genotype persisted as an independent predictor of complicated lesions ( P=0.007) and coronary thrombosis. In conclusion, the ESR1 gene is a potential candidate behind the pathogenesis of acute coronary events.
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PMID:Coronary artery wall atherosclerosis in relation to the estrogen receptor 1 gene polymorphism: an autopsy study. 1189 38

Estrogen receptors (ERs) are considered to mediate the ability of 17beta-estradiol (estradiol) to reduce injury-induced proliferation of vascular smooth muscle cells (VSMCs), leading to vascular lesions. However, the finding that estradiol attenuates formation of vascular lesions in response to vascular injury in knockout mice that lack either ER-alpha or ER-beta challenges this concept. Our hypothesis is that the local metabolism of estradiol to methoxyestradiols, metabolites of estradiol with little affinity for ERs, mediates the ER-independent antimitogenic effects of estradiol on VSMCs. In human VSMCs, 2-methoxyestradiol and 2-hydroxyestradiol were more potent than was estradiol in inhibiting DNA synthesis (3[H]-thymidine incorporation), collagen synthesis (3[H]-proline incorporation), cell proliferation (cell number), and cell migration (movement of cells across a polycarbonate membrane). The inhibitory effects of estradiol on VSMCs were enhanced by cytochrome-P450 (CYP450) inducers 3-methylcholanthrene and phenobarbital. Moreover, the inhibitory effects of estradiol were blocked in the presence of the CYP450 inhibitor 1-aminobenzotriazole and the catechol-O-methyltransferase inhibitors quercetin and OR486. Both OR486 and quercetin blocked the conversion of 2-hydroxyestradiol to 2-methoxyestradiol; moreover, they blocked the antimitogenic effects of 2-hydroxyestradiol but not of 2-methoxyestradiol. The ER antagonist ICI182780 blocked the inhibitor effects of estradiol on VSMCs, but only at concentrations (>50 micromol/L) that also inhibit the metabolism of estradiol to hydroxyestradiols (precursors of methoxyestradiols). In conclusion, the inhibitory effects of locally applied estradiol on human VSMCs are mediated via a novel ER-independent mechanism involving estradiol metabolism. These findings imply that vascular estradiol metabolism may be an important determinant of the cardiovascular protective effects of estradiol and that nonfeminizing estradiol metabolites may confer cardiovascular protection regardless of gender.
Hypertension 2002 Apr
PMID:Methoxyestradiols mediate estradiol-induced antimitogenesis in human aortic SMCs. 1196 42

Hypertrichosis, characterized by increased hair growth located in non-androgen-dependent areas, does not justify the monitoring of hormone levels, conversely to hirsutism, with increased hair growth in androgen-dependent areas of the female genitals. Adult hypertrichosis is iatrogenic (minoxidil, ciclosporine, diazoxide or glucocorticosteroids), of metabolic origin (porphyria), nutritional (anorexia) or paraneoplastic (hypertrichosis lanuoginosa). Metabolic or general assessment can help clinical diagnosis. In non-iatrogenic hirsutism the following must be eliminated: 1) a virilizing tumor (ovarian, adrenal) when confronted with rapid progression or recent hirsutism, plasma testosterone (T)>1.5ng/ml and/or (adrenal tumor) DHEA-sulfate (DHEAS)>700 microgram/dl and associated with hypertension; 2) when confronted with characteristic signs of hirsutism, Cushing's syndrome (post-dexamethasone cortisol), hyperprolactinemia (pooled PRL), or acromegalia (IGF1). Measurement of 17-OH-progesterone at 8 am on the 4th day of the cycle detects the late manifestation homozygous forms of a 21-hydroxylase (21OHD) block. The more frequent forms are: 1) ovarian polymicrocystic or hirsutism-anovulation syndromes without other causes (LH/FSH, T, hyperinsulinemia, sonography); 2) functional adrenal hyperandrogenia (increased DHEAS without organic cause); 3) idiopathic hirsutism. Treatment can be local (discoloration, depilation, diathermo-coagulation, laser). Treatment of hirsutism of organic origin is etiologic. The inhibitory effects of glucocorticosteroids are mediated by 21OHD. The most effective treatments are anti-androgenic: cyproterone acetate, progesterone-like and anti-gonadotropic (contraceptive) agents; and the only product in France officially indicated in hirsutism , spironolactone (anti-mineralocorticosteroid); and flutamide, pure anti-androgen (probably hepatoxic). Finasteride (type II 5 alpha-reductase inhibitor) appears less effective. Estrogen-progestagen-like agents can be associated with anti-androgens. We should also mention the GnRH-agonists, and finally, dietetics and metformine (in cases of insulin-resistance).
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PMID:[Hirsutism and hypertrichosis in adults: investigations and treatment]. 1222 63

The risks of steroidal contraception as reviewed by the Central Medical Committee of the International Planned Parenthood Federation in April 1970 are presented and discussed. The causal relationship between the use of steroidal contraceptives and thromboembolic disease is accepted, but the complication is considered very rare. It is recommended that oral formulations containing less than 50 micrograms of estrogen be used wherever possible, but for those women who need a higher estrogen content, it is still responsible to prescribe it. No adequate evidence has been obtained linking steroidal contraception in any relationship with cancer or fetal abnormalities. Estrogen administration possibly produces an adverse change in the quantity and quality of milk and the duration of lactation. Rare cases of jaundice and hypertension appear to be sometimes associated with oral contraceptive use and are easily reversible. Changes in glucose tolerance and serum lipids appear to occur under steroidal administration and are reversible. It is possible that those women with a history of irregular menstruation prior to taking the pill may experience prolonged anovulation after ceasing pill use. Mental changes reported due to oral contraceptives are highly subjective in nature and difficult to evaluate. It is concluded that the pill is highly effective as a method of family planning and is a significant factor in world health presenting no risks that justify discontinuation of its use.
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PMID:Use of steroidal contraception justified. 1225 54

There are hormones from 2 sources which determine the menstrual cycle. The pituitary produces luteinizing hormone and follicle stimulating hormone and the ovaries secrete estrogen and progesterone. For clinical use, a cheap source of progesterone has been found in the Mexican yam. Since the 1st oral contraceptives were tested in Puerto Rico in the late 1950s, there has been a trend toward reducing the dosage. Estrogen prevents ovulation in 95-98% of patients. Other factors are also involved. Although it is estimated that 80-100 million women in the world today use oral contraceptives, this method is not always followed for long periods. From 25 to 60% discontinue the use within the 1st year. Increased risk of unfavorable side effects occurs in those with high blood pressure, migraine headaches, diabetes, epilepsy, undiagnosed genital bleeding, or gallbladder disease. Women over age 40 run a greater risk of heart attacks. Intravenous blood clots are the major risk. Severe abdominal, chest, or leg pains, severe headaches, and eye problems may be symptoms of blood clots. With the 21-day package the user takes a pill a day for 3 weeks and then none during menstruation. The sequential type of medication is no longer used. Minipills are taken every day. Missing taking pills is the most common cause of failure of the method. Estrogen replacement therapy for menopausal women is a temporary treatment to relieve physical distress. Depo-Provera, containing a long-acting progesterone agent, may be injected every 3 months instead of daily oral contraceptives. When progesterone is used with an IUD it acts locally. Hormones to maintain pregnancy are no longer used. Use of hormones as a test for pregnancy has been discontinued. Estrogen-progesterone injections given to inhibit milk production may cause serious side effects.
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PMID:The pills: oral contraceptives and other hormones. 1230 26

The effect of quinestrol compound on fat metabolism in 206 women who took quinestrol compound for 5-13 years and in 159 controls was studied. The blood concentration of CL, TG, and FFA was examined in each of the cases and controls. The value of every indicator in fat metabolism of the cases who took quinestrol compound for 5 years was markedly higher than in the controls (p0.001 in cholesterol, p0.05 in B-LP, p0.01 in HDL). The effect of oral contraceptives (OCs) consisting of estrogen and progesterone on fat metabolism were dependent on the type and dosage of steroids. Estrogen was associated with an increase of CL, HDL-CL, and a decrease of LDL-CL, while progesterone has little effect on the level of blood fat. The elevated CL and TG level is believed to be associated with cardio vascular disease, while a higher level of HDL is protective against the disease. Therefore, precautions should be taken with longterm use of estrogen, especially with large doses as substantially higher levels of TG and FFA were found in longterm rather than in shortterm users, while the difference in HDl was not as big. It was suggested that clients with a high level of blood fat, high blood pressure, and liver disease should choose alternative contraceptive methods and users of OCs should switch to other methods after 5 years.
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PMID:[Effect of compound quinestrol on fat metabolism]. 1231 89

Although combined oral contraceptives (OCs) do not create a true cardiovascular risk, they may increase the impact of existing vascular risk factors. Pill use disturbs metabolism of lipids and carbohydrates as well as the balance of water and sodium. New combinations with lower doses of steroids have significantly reduced these risks, and the development of new and less androgenic progestins for low dose pills is expected to reduce them further. The diabetogenic effect of OCs has been noted since 1963. Among normal women, the observed modifications in carbohydrate metabolism are minor and temporary, with increases in levels of blood sugar maximal at the beginning of use and normalizing after 12 months. Among women with family histories of diabetes or who have had gestational diabetes, use of combined OCs can entail irreversible deterioration of glucose tolerance or diabetes. The number of women with poor glucose tolerance increases with the duration of pill use. Reversibility of the condition decreases with duration of use. The proportion of women with poor glucose tolerance who develop diabetes is higher than among normal subjects. Women with poor glucose tolerance must be considered at risk of diabetes. Ethinyl estradiol is responsible for the early modification of glucose tolerance, which regresses after about 6 months of use. Hyperinsulinemia is caused by the direct stimulation of progestins on insulin secretion by the pancreas as well as by the development of peripheral resistence to glucose utilization resulting from a decrease of insulin receptors. The effect on insulin resistence is among the most androgenic progestins. Chronic hyperinsulinism represents a classic risk factor for atherosclerosis because of the effects on the arterial wall: proliferation of smooth muscle fibers, inhibition of lipolysis, and development of lesions of the intima analogous to those of atheroma. Estrogen is primarily responsible for the increased blood pressure of pill users, but the development of hypertension is also correlated with the progestin content. Progestins have an antidiuretic effect which contributes to increases in blood pressure when added to the estrogen stimulation of the renin-aldosterone-angiotensin system. Gestodene, a new progestin in the gonane series, is the most powerful synthetic progesterone yet known. Its uniqueness derives from the dissociation between its very powerful antigonadotropic activity even at small doses and its androgenic effects which only appear at considerably higher doses. Most of the metabolic effects of progestins are linked to their degree of androgenicity. Different studies of gestodene tolerance in a triphasic formulation have concluded that it is innocuous. The use of gestodene in a low-dose triphasic formulation may result in a combined OC that does not increase the individual atheromatous risk of the user.
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PMID:[Combined estrogen-progestagen contraception and glucid and water-sodium metabolism]. 1234 1

A recent study shows that estrogens protect the female heart from the hypertrophy resulting from disturbance of myocardial calcium metabolism. Estrogens can inhibit cardiac hypertrophy by counteracting hypertension, by direct effects on the heart and by triggering the release of cardioprotective factors. However, because the hypertrophic response to increased cardiac load is primarily an adaptive process, the inhibition of hypertrophy might not always be beneficial. Estrogen therapy could interfere with the utilization of the larger hypertrophic reserve in the female heart, and predispose the female heart to systolic dysfunction.
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PMID:Gender matters: estrogen protects from cardiac hypertrophy. 1259 Nov 69


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