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

Vasoprotective drugs decrease the vulnerability of blood vessels to cardiovascular risk factors such as hypertension and hypercholesterolemia. Mechanistic treatment end-points of hypertension (normalization of endovascular pressure) may not correct nonhypertensive components of the pathobiology of hypertension. Estrogen replacement therapy, antihypertensive treatment with angiotensin-converting enzyme inhibitors, and manipulations of nitric oxide metabolism may have beneficial effects on vessels in the absence of blood pressure normalization. Estrogens and L-arginine, the precursor of nitric oxide, can partly correct impaired endothelium-dependent vasodilation, a pathophysiologic hallmark of hypertensive states. Angiotensin-converting enzyme inhibitors preserve endothelium-dependent vasodilation and protect arteries against the atherogenic effects of hypercholesterolemia by a non-hypolipidemic, non-hypotensive mechanism.
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PMID:Vasoprotection and antihypertensive therapy. 760 51

Postmenopausal women are 2-3 times more likely to have a heart attack than premenopausal women. According to the results of the Framingham study, angina is one of the main manifestations of coronary heart disease in women, whereas myocardial infarction and sudden death are more frequent in men. Cigarette smoking, high blood pressure and hypercholesterolemia are major risk factors for coronary heart disease in both men and women, while diabetes mellitus and hypo-high-density lipoproteinemia are more clearly associated with cardiovascular disease in women than in men. Endogenous and exogenous hormones may be a major determinant of the cardiovascular risk in women. Premenopausal women have a considerably lower incidence of coronary heart disease than postmenopausal women, and estrogen therapy is associated with a reduced risk in the latter. Part of this protective effect seems to be due to the influence of estrogen therapy on lipoprotein metabolism, i.e. a decrease in LDL cholesterol and an increase in HDL cholesterol. Progestins, to an extent which depends on their androgenic potency, have the opposite effects. A large study (the Postmenpausal Estrogen Progestin Intervention Trial) has been launched to test the effect of the estrogen-progestin combination on various cardiovascular risk factors.
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PMID:Estrogens and progestins in postmenopausal women: influence on lipid parameters and cardiovascular risk. 772 Dec 54

Elevated insulin concentrations are frequently found in both men and women with coronary heart disease (CHD), and are likely to be due to insulin resistance. Hyperinsulinaemia may increase CHD risk by directly promoting atherogenesis, and insulin propeptides may also be important in this respect. However, increased insulin concentrations may adversely affect several other CHD risk factors, and it has been postulated that insulin resistance is a pivotal metabolic disturbance in a constellation of CHD risk factors. There is an association between hyperinsulinaemia and hypertension, although it is not known if this association is direct. Increased insulin concentrations are also associated with high triglycerides, low HDL or HDL2 concentrations, and increased small dense LDL. Obesity is also associated with insulin resistance, and it is the central or android body fat distribution which correlates with these metabolic disturbances. All these associated factors constitute a distinct syndrome--the insulin resistance syndrome--which is a frequent finding in patients with CHD, including microvascular angina. It is possible that the adverse associations of insulin resistance and dyslipidaemia are mediated through increased nonesterified fatty acid flux. Increased insulin levels are also associated with increases in the anti-fibrinolytic factor, plasminogen activator inhibitor-I (PAI-I). Whilst increased insulin levels are typically associated with insulin resistance, reduced hepatic insulin uptake may also be important. We now have techniques which can quantitate insulin secretion, hepatic uptake and release, elimination, and resistance. The menopause has appreciable effect on insulin and glucose metabolism. Estrogen and progesterone augment pancreatic insulin secretion, but the former reduces insulin resistance whilst the latter increases it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HRT mechanisms of action: carbohydrates. 819 41

It has been demonstrated that high cholesterol levels are correlated with development of atherosclerosis, while high levels of high density lipoprotein (HDL) are associated with reduced cardiovascular mortality. Some endocrine disorders accelerate atherosclerosis in association with hypercholesterolemia, hypertension, low level of HDL and hypertriglyceridemia. In patients with acromegaly, hypertriglyceridemia is sometimes accompanied with and aggravated by the presence of impaired glucose tolerance. In patients with hypothyroidism, coronary atherosclerosis may develop in association with hypertension, hypercholesterolemia and moderate elevation of triglyceride which is often accumulation of intermediate lipoprotein. Cushing syndrome may accelerate atherosclerosis by the fact that corticosteroid may induce or exacerbate several known coronary risk factors including hypertension, hypercholesterolemia and impaired glucose tolerance. Estrogen has beneficial effects on the cardiovascular system for postmenopausal women by affecting lipid metabolism, decrease of LDL and increase of HDL.
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PMID:[Atherosclerosis and endocrine disorders]. 841 91

Widespread application of proven primary and secondary preventive strategies for coronary heart disease would result in substantial savings of life and health care dollars. Proven strategies (excluding lipid therapy) include quitting smoking, treating hypertension, physical activity, aspirin therapy, and appropriate use of anticoagulants, beta blockers, and angiotensin-converting enzyme inhibitors in survivors of myocardial infarction. Estrogen replacement therapy is currently under clinical investigation. Avoidance of obesity and tight control of diabetes are prudent interventions as yet unproved by clinical trials. Unfortunately, preventive strategies are frequently underutilized. The greatest challenge for preventive cardiology is to put into practice what we already know to prevent the development and progression of atherosclerosis.
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PMID:Nonlipid primary and secondary prevention strategies for coronary heart disease. 872 3

The mechanisms of estrogen-induced cardiovascular protection are incompletely understood. Acute estrogen administration enhances acetylcholine-induced vasorelaxation, suggesting that endothelium-dependent factors may be important. The effect of long-term estrogen supplementation on endothelial function has not been well defined. In this double-blind, randomized study, we examined endothelial function in forearm resistance arteries in 11 perimenopausal women before and after 8 weeks of estrogen supplementation (estradiol valerate, 2 mg daily, n = 6) 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 influence blood pressure or heart rate. Estrogen supplementation significantly reduced systolic and diastolic pressures but had no effect on plasma lipoproteins. Estrogen did not alter the vasodilator responses to acetylcholine at doses of 9.25, 18.5, and 37 micrograms/min (rise in forearm blood flow before estrogen: 263 +/- 72%, 288 +/- 66%, and 383 +/- 84%, respectively; after estrogen: 205 +/- 34%, 260 +/- 44%, and 359 +/- 54%, P > .05.). Vasodilator responses to the endothelium-independent agent sodium nitroprusside (1.6 micrograms/min) were also unchanged after estrogen supplementation. However, estrogen enhanced vasoconstrictor responses to the nitric oxide synthase inhibitor NG-mono-methyl-L-arginine at doses of 1, 2, and 4 mumol/min (fall in fore-arm blood flow before estrogen: 13 +/- 9%, 20 +/- 7%, and 26 +/- 8%, respectively; after estrogen: 18 +/- 9%, 36 +/- 7%, and 47 +/- 7%, P = .04). Responses to vasoactive agents were unchanged after administration of placebo. Thus, in perimenopausal women, estrogen supplementation reduces blood pressure and enhances basal but not acetylcholine-induced nitric oxide release in fore-arm resistance arteries.
Hypertension 1996 Sep
PMID:Estrogen enhances basal nitric oxide release in the forearm vasculature in perimenopausal women. 918 Jun 41

Cardiovascular disease is the leading cause of death among women, yet clinical trials have not evaluated specific treatment strategies for women. Recently, there has been an expansion of scientific literature exploring differences between women and men with hypertension and cardiovascular disease. The cardioprotective effects of estrogen have been well demonstrated, and the loss of endogenous estrogens with aging contributes to the rapid increase in the incidence of coronary artery disease after menopause. Many of the adverse effects of estrogen deficiency are reversible with estrogen replacement. Estrogen improves lipoprotein profiles, has vasodilatory effects on the endothelium, and inhibits vascular smooth muscle cell growth and constriction. These effects likely all contribute to the reduction in coronary artery disease in the presence of estrogen, and the clinical benefits are not attenuated by concurrent progestins. There are gender-specific differences in the epidemiology of hypertension and coronary artery disease, as well as differences in the pathophysiology and clinical manifestations of disease. Given important experimental interactions between estrogens and the major classes of antihypertensive agents, as well as secondary benefits such as a possible reduction in bone loss with certain agents, a gender-specific approach to hypertension appears to be warranted. Future clinical trials will need to address gender-specific differences in treatment approaches.
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PMID:Gender considerations in hypertension pathophysiology and treatment. 887 71

2-Hydroxylation is one of the major metabolic pathways of estrogens and is believed to be catalyzed by a form of cytochrome P450. Recently it has been reported that estrogen 2-hydroxylase activity in human placenta is catalyzed by aromatase. Some investigators suggested the effect of catechol estrogen on human placental steroidogenesis which may be related to pregnancy-induced hypertension (PIH) through the inhibition of catechol-O-methyltransferase (COMT) activity. In order to better understand the interrelationship between placental aromatase and estrogen 2-hydroxylase activities in PIH patients, both activities were evaluated in the PIH placentas. Human placental microsomes obtained from PIH patients were incubated with [1 beta-3H]androstenedione or [2-3H]estradiol in the presence of NADPH. Aromatase and estrogen 2-hydroxylase activities were assessed by the tritium water method. The immunosuppression patterns of both activities due to monoclonal antiaromatase cytochrome P450 antibody (MAb3-2C2) were studied. Estrogen 2-hydroxylase activity was significantly higher in PIH placentas (4.7 +/- 0.9 pmol/min/mg protein, n = 7) than in normal placentas (3.0 +/- 0.7 pmol/min/mg protein, n = 7). When the PIH placental microsomes were subjected to immunosuppression by 1 to 100 micrograms IgG of MAb3-2C2, estrogen 2-hydroxylase activity was suppressed by 94 to 65% whereas aromatase activity was strongly suppressed by 72 to 17%, respectively. From our results of high estrogen 2-hydroxylase activity in PIH placentas, it is assumed that there is a different estrogen catalyzing mechanism in PIH placentas.
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PMID:Aromatase and estrogen 2-hydroxylase activities of human placental microsomes in pregnancy-induced hypertension. 893 May 23

This study was designed to characterize the hemodynamic and biochemical properties of the abdominal aorta in four genetically related inbred rat strains that express genetic hypertension and hyperactive behavior in varying combinations. These include (1) the spontaneously hypertensive rat (SHR), which is hypertensive, hyperactive, and hyperreactive to stress; (2) Wistar-Kyoto (WKY) rats, which express none of these traits; (3) WKHT rats, which are hypertensive but not hyperactive; and (4) WKHA rats, which are hyperactive and hyperreactive to stress, but normotensive. Together, these four strains allowed us to examine the structural and functional changes in the aorta in the hypertensive SHR, the most widely used animal model of genetic hypertension, while controlling for the variables of hyperactivity and hyperreactivity that are also expressed in the SHR. Four groups of animals of both sexes were studied: (1) WKY, n = 101, (2) WKHA, n = 33, (3) WKHT, n = 91, and (4) SHR, n = 28. Blood pressure (BP) was determined by tail plethysmography as well as direct intraarterial monitoring under anesthesia. Fixed specimens were prepared for histologic analysis and the wall thickness determined morphometrically. Quantification of soluble tissue protein, elastin, and collagen in the aortic tissue was determined by measuring leucine (leu), hydroxyproline (HP/leu), and desmosine (DES/leu). The hypertensive strains (SHR and WKHT) had significantly higher tail BP than the normotensive strains (WKY and WKHA)-WKY: 128.7 +/- 22.3; WKHA: 126.7 +/- 14.6; WKHT: 162.8 +/- 21.2; SHR: 164.2 +/- 36.1 (p < 0.0001). Additionally, intraaortic diastolic BP and mean BP were higher in SHR rats than in WKHT. Morphometric studies showed the media thickness in the SHR rats was significantly greater than in the WKY and WKHA rats and no different than in the WKHT rats. Significantly less of the aortic wall protein was present as elastin in the hypertensive rats (SHR and WKHT), as well as the hyperactive rats (WKHA), compared to rats that had neither trait (WKY). These studies provide new information regarding aortic structure and function in genetic hypertension using inbred strains to control for the hyperactivity/hyperreactivity traits that coexist with hypertension in the SHR. They reveal that hypertensive aortas have altered matrix proteins that cannot be explained simply on the basis of blood pressure alone.
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PMID:Hemodynamic and biochemical characteristics of the aorta in the WKY, SHR, WKHT, and WKHA rat strains. 895 87

We have previously shown that juvenile Sprague-Dawley rats, fed a diet in which complex carbohydrates are replaced by sucrose, develop insulin resistance and hypertension. These conditions develop despite the absence of genetic predisposition to either. When studied with the euglycemic hyperinsulinemic clamp technique, these rats have reduced insulin-stimulated glucose utilization, but normal suppression of hepatic glucose output. In the young sucrose-fed rats, it was noted that the degree of blood pressure elevation was greater in males than in females. The purpose of this study was to test the hypothesis that estrogen withdrawal increases insulin resistance and hypertension. Female rats were randomized at weaning (3 weeks of life) to receive control diet or sucrose diet. Animals were assessed with weekly weight and indirect tail-cuff blood pressure. At 8 weeks of life, the sucrose-fed rats were randomized to receive bilateral oophorectomy or sham surgery (anesthesia and uterine horn exposure without removal of the ovaries). At 13 to 14 weeks of life, all animals were fasted overnight, and had an oral glucose tolerance test while conscious. Weight and weight gain were not different among the groups over the 11 week study period. Animals fed the sucrose diet developed significantly higher blood pressure than animals fed the control diet; oophorectomized animals had higher blood pressure than sham-operated animals (P <.0001). Sucrose-fed oophorectomized animals developed fasting and glucose-stimulated hyperinsulinemia. Estrogen withdrawal augments blood pressure in juvenile rats made insulin resistant and hypertensive with a sucrose diet. Estrogen withdrawal in these animals also induces fasting and glucose-stimulated hyperinsulinemia, which are signs of worsening insulin resistance. Androgen:estrogen imbalance increases metabolic dysfunction and worsens hypertension in this animal model.
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PMID:Effect of estrogen withdrawal on blood pressure and insulin resistance in sucrose-fed juvenile rats. 897 91


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