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PubMed2004

Effects of HMG-CoA reductase inhibitors on endothelial function: role of microdomains and oxidative stress.

Certain pleiotropic activities reported for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are related to reductions in cellular cholesterol biosynthesis and isoprenoid levels. In endothelial cells, these metabolic changes contribute to favorable effects on nitric oxide (NO) bioavailability. Given the essential role of NO in preserving vascular structure and function, this effect of statins is of considerable therapeutic importance. Statins have been demonstrated to restore endothelial NO production by several mechanisms, including upregulating endothelial NO synthase (eNOS) protein expression and blocking formation of reactive oxygen species. In this article, we will discuss additional ways in which statins restore endothelial NO production and improve endothelial function. (1) Statins modulate membrane microdomain formation, resulting in reduced expression of proteins that specifically inhibit eNOS activation. (2) Statins reduce sterol biosynthesis, thus interfering with the formation of pathologic microdomains, including cholesterol crystalline structures. This observation has important implications for plaque stabilization, as these microdomains contribute to cholesterol crystal formation and endothelial apoptosis. Finally, (3) statins improve endothelial function by interfering with oxidative stress pathways through both enzymatic and nonenzymatic mechanisms. The relationships between membrane microdomains, cholesterol biosynthesis, and endothelial function will be discussed.

Animals↗

PubMed2003

Assessing endothelial function as a risk factor for cardiovascular disease.

The vascular endothelium plays a key role in the prevention of atherosclerosis. Endothelial dysfunction is an antecedent of clinical cardiovascular disease and can be viewed as the final pathway between coronary risk factors and the development of atherosclerosis. The development of a noninvasive method of assessing endothelial health (ie, measurement of flow- mediated dilation of the brachial artery) has enabled investigators to evaluate the effects of dietary patterns on vascular function. Emerging evidence indicates that dietary fats may acutely impair endothelial function, but this effect is dependent on the type of fat and on the other nutrients consumed. Although inconclusive, studies in cohorts of modest size suggest that antioxidants, L-arginine, and folic acid may modulate endothelial function. Additional research is needed to define the impact of complex, long-term dietary patterns on the vascular endothelium.

Antioxidants↗

PubMed2006

The oestrogen receptor beta contributes to sex related differences in endothelial function of murine small arteries via EDHF.

Sex related differences in cardiovascular function have been reported in oestrogen receptor beta knockout (ERbetaKO) mice. In this study we examined the role of endothelium-derived hyperpolarizing factor (EDHF) in differences in small artery endothelial function between ERbetaKO and wild-type (WT) mice. Small femoral arteries were isolated from ERbetaKO and WT mice and mounted on a wire myograph. Concentration-response curves to ACh were compared before and after incubation with inhibitors of nitric oxide (NO) and prostacyclin (PGI2) synthesis. Comparison of the expression of the principal vascular connexins (Cx37, 40 and 43), implicated in EDHF-mediated dilatation were undertaken by immunohistochemistry. Vascular ultrastructure was studied by transmission and scanning electron microscopy. ACh-induced relaxation of arteries (< 200 microm internal diameter) was greater in WT females versus males and was attributable to a greater EDHF component of relaxation. This sex difference was absent in ERbetaKO mice. Arteries from ERbetaKO males (but not females) were more sensitive to ACh compared to WT. The pharmacological evidence and morphological prerequisite for involvement of gap junctions in EDHF-mediated responses was confirmed in male arteries. The absence of ERbeta had no influence on expression of main Cx subtypes within vascular wall or on ultrastructure and morphology of the endothelium. The data suggest that in WT male mice, ERbeta reduces EDHF-mediated relaxation through gap junction communication.

Acetylcholine↗

PubMed2004

[Clinical significance of the assessment of endothelial function].

Endothelium-derived nitric oxide is not only a potent vasodilator but also inhibits platelet aggregation, vascular smooth muscle cell migration and proliferation, monocyte adhesion and adhesion molecule expression, thus protecting the vessel wall from the development of atherosclerosis and thrombosis. Major cardiovascular risk factors are associated with endothelial dysfunction, which involves enhanced production of oxygen free radicals, that can destroy nitric oxide and reduce its availability, and release of endothelium-derived contracting factors including prostanoids and endothelin-1. Endothelial dysfunction is a promoter of atherosclerotic and thrombotic damage and in prospective studies on patients with high cardiovascular risk impaired endothelium-dependent vasodilation is associated with an increased incidence of cardiovascular events. However, endothelial function cannot yet be included among the surrogate endpoints which need to be measured for cardiovascular risk stratification. This limitation springs from the fact that available tests to assess endothelium-dependent vasodilation are invasive or, if noninvasive, they have no sufficient sensitivity and specificity to be proposed for clinical practice. Moreover, no study is available demonstrating that reversal of endothelial dysfunction, which can be obtained by appropriate treatment, is independently associated with a better clinical outcome. However it is conceivable that in the future, by the utilization of a non-invasive method such as the determination of brachial artery flow-mediated dilation, large-scale multicenter trials might provide a definitive answer to the real prognostic value of endothelial dysfunction, in terms of cardiovascular risk and therapeutic approach.

Cardiovascular Diseases↗

PubMed2006

The association between right coronary artery morphology and endothelial function.

BACKGROUND: Two distinct right coronary artery (RCA) morphologies have been previously described: sigma- and C-shaped RCAs. While the C-shaped RCA was significantly associated with atherosclerosis, the sigma-shaped was not. The association of RCA morphology and vascular endothelial function has not yet been assessed. METHODS: To evaluate the association between the RCA's morphology and flow-mediated endothelium-dependent dilation (FMD) in patients without evidence of atherosclerotic lesions, we prospectively assessed FMD in 49 consecutive patients with non-specific chest pain, who were referred to our laboratory 30+/-10 days after corroboration of normal coronary arteries on coronary angiography. Endothelium-dependent brachial artery FMD and endothelium-independent nitroglycerin-mediated vasodilation (NTG) were assessed using high resolution (15 MHz) linear array ultrasound. The patients were divided into 2 groups according to their RCA morphology on coronary angiograms (sigma and C) which were analyzed by 2 independent readers who were blinded to the patients' FMD results. RESULTS: The C-shaped group exhibited a significantly lower FMD compared to the sigma-shaped group (9.0+/-4.2% vs. 14.3+/-4.7%, p<0.04, respectively), while NTG was the same in both groups. There were no significant group differences in other variables. CONCLUSIONS: Endothelium-dependent FMD in the brachial artery is significantly greater in sigma- compared to C-shaped RCA in coronary arteries without overt atherosclerotic lesions, suggesting a potential mechanism whereby C-shaped RCA are predisposed to atherosclerosis.

Aged↗

PubMed2000

Effect of the angiotensin II type 1 receptor blocker candesartan on endothelial function in patients with essential hypertension.

Patients with essential hypertension are characterized by impaired basal and agonist-evoked nitric oxide release and increased endogenous endothelin (ET)-1-induced vasoconstriction. To assess whether candesartan, an angiotensin II type 1 receptor blocker, can improve endothelial function, we studied the changes in forearm blood flow (FBF) induced in 15 hypertensive patients and in 15 control subjects by the intrabrachial infusion of N(G)-monomethyl-L-arginine (L-NMMA), norepinephrine, the ET A/B receptor antagonist TAK 044, sodium nitroprusside, and acetylcholine. In hypertensive patients, the FBF study was repeated 2 and 12 months after the start of treatment with candesartan cilexetil (8 to 16 mg daily). Compared with controls (maximal FBF decrease, -46+/-11%), hypertensive patients showed a reduced (P<0.001) vasoconstrictor response to L-NMMA (maximal FBF decrease, -28+/-7%); the response to norepinephrine was only slightly impaired, and the response to sodium nitroprusside was similar to that of controls. Finally, TAK-044 caused greater vasodilation in hypertensive patients (maximal FBF increase, 77+/-9%) than in controls (maximal FBF increase, 17+/-10%). In hypertensive patients, candesartan cilexetil significantly enhanced vasoconstriction to L-NMMA after 2 and 12 months (maximal FBF decrease, 37+/-2% [P<0.05] and 42+/-2% [P<0.001], respectively). The responses to norepinephrine, acetylcholine, and sodium nitroprusside were not modified after 2 months. After 12 months, the responses to acetylcholine and sodium nitroprusside were significantly (P<0.05) enhanced at the highest rates. Vasodilation to TAK-044 was abolished after treatment with candesartan cilexetil; this effect is associated with a reduced plasma ET-1 concentration. This study demonstrated that the angiotensin II receptor blocker candesartan improves tonic nitric oxide release and reduces vasoconstriction to endogenous ET-1 in the forearm of hypertensive patients.

Acetylcholine↗

PubMed2003

Angiotensin II produces superoxide-mediated impairment of endothelial function in cerebral arterioles.

BACKGROUND AND PURPOSE: Angiotensin II (Ang II) produces oxidative stress in vascular cells in culture and in extracranial conduit arteries. The goal of this study was to examine the hypothesis that Ang II produces superoxide-mediated impairment of endothelial function in cerebral microvessels. METHODS: Diameter of cerebral arterioles (baseline diameter=104+/-3 microm) was measured with the use of a closed cranial window in anesthetized rabbits. Topical application of Ang II was used to avoid effects on arterial pressure. RESULTS: Ang II (0.1 to 1 micromol/L for 2 hours) had no effect on baseline diameter (change in diameter of -3+/-2% in response to 1 micromol/L Ang II) but produced concentration-dependent inhibition of vasodilatation to the endothelium-dependent agonist bradykinin. For example, 1 micromol/L Ang II inhibited responses to 1 nmol/L bradykinin by almost 80%. These inhibitory effects of Ang II were prevented by the superoxide scavenger 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron; 10 mmol/L) or diphenylene iodonium (DPI; 3 micromol/L), an inhibitor of NAD(P)H oxidase. Ang II did not inhibit vasodilatation in response to nitroprusside, an endothelium-independent vasodilator. CONCLUSIONS: These findings are the first evidence that local Ang II produces superoxide-mediated vascular dysfunction in cerebral microvessels. The results with DPI suggest that the source of superoxide may be an NAD(P)H oxidase.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

PubMed1999

Exercise training enhances endothelial function in young men.

OBJECTIVES: The present study was designed to assess whether exercise training can enhance endothelium-dependent dilatation in healthy young men. BACKGROUND: Exercise has been shown to reduce cardiovascular morbidity and mortality, but the mechanisms for this benefit are unclear. Endothelial dysfunction is an early event in atherogenesis, and animal studies have shown that exercise training can enhance endothelial function. METHODS: We have examined the effect of a standardized, 10-week, aerobic and anaerobic exercise training program on arterial physiology in 25 healthy male military recruits, aged 17 to 24 (mean 20) years, of average fitness levels. Each subject was studied before starting, and after completing the exercise program. Baseline vascular reactivity was compared with that of 20 matched civilian controls. At each visit, the diameter of the right brachial artery was measured at rest, during reactive hyperemia (increased flow causing endothelium-dependent dilation) and after sublingual glyceryltrinitrate (GTN; an endothelium-independent dilator), using high-resolution external vascular ultrasound. RESULTS: At baseline, flow-mediated dilatation (FMD) and GTN-mediated dilatation were similar in the exercise and control groups (FMD 2.2+/-2.4% and 2.4+/-2.8%, respectively, p = 0.33; GTN 13.4+/-6.2 vs. 16.7+/-5.9, respectively, p = 0.53). In the military recruits, FMD improved from 2.2+/-2.4% to 3.9+/-2.5% (p = 0.01), with no change in the GTN-mediated dilation (13.4+/-6.2% vs. 13.9+/-5.8%, p = 0.31) following the exercise program. CONCLUSION: Exercise training enhances endothelium-dependent dilation in young men of average fitness. This may contribute to the benefit of regular exercise in preventing cardiovascular disease.

Administration, Sublingual↗

PubMed2005

Blood pressure circadian rhythm and endothelial function in heavy smokers: acute effects of transdermal nicotine.

Nicotine replacement therapy appears to be safe when used by healthy patients to aid in smoking cessation; however, the immediate acute effects of nicotine replacement therapy on the circadian rhythm of blood pressure (BP) and endothelial function in heavy smokers are not well understood. Twenty-six heavy smokers were requested to stop smoking for 48 hours. BP and heart rate were recorded over 48 hours by ambulatory BP monitoring, with beat-to-beat changes being monitored for the first 10 hours by a noninvasive finger device. The reactivity of the brachial artery was evaluated using flow-mediated dilation immediately after smoking cessation, before the application of a 21-mg nicotine patch or placebo patch, and 24 hours after patch placement. Transdermal nicotine caused a mild but significant elevation in BP in the early morning in 21 of 26 volunteers. The decrease in nocturnal BP was attenuated in patients with the nicotine patch compared with the placebo patch; this was associated with impaired endothelium-dependent vasodilation.

Administration, Cutaneous↗

PubMed1996

[Sympathetic nervous system and endothelial function in heart failure].

Congestive heart failure is a frequent cardiovascular disease with a poor prognosis in advanced stages. Activation of neurohumoral systems such as the renin-angiotensin system and the sympathetic nervous system as well as impairment of local regulatory mechanisms (i.e. adrenoceptors, endothelial factors) play an important role in the pathogenesis and prognosis of the disease. The increase in peripheral resistance is due to imbalance of vasoconstrictors and vasodilators in favour of the vasoconstrictors and to changes in endothelial function, i.e. impaired production of nitric oxide, increased production of endothelin. Sodium and volume retention as well as the activation of the renin-angiotensin system increase preload. The sympathetic nervous system, which is known to be an independent negative prognostic factor, is activated and interacts with the renin-angiotensin system; however, up to now it is uncertain, whether these pathophysiological findings contribute to the development of congestive heart failure or if they are only secondary phenomena.

Amino Acid Sequence↗

PubMed2003

Normal insulin-stimulated endothelial function and impaired insulin-stimulated muscle glucose uptake in young adults with low birth weight.

Low birth weight has been linked to insulin resistance and cardiovascular disease. We hypothesized that insulin sensitivity of both muscle and vascular tissues were impaired in young men with low birth weight. Blood flow was measured by venous occlusion plethysmography during dose-response studies of acetylcholine and sodium nitroprusside in the forearm of fourteen 21-yr-old men with low birth weight and 16 controls of normal birth weight. Glucose uptake was measured during intraarterial insulin infusion. Dose-response studies were repeated during insulin infusion. The maximal blood flow during acetylcholine infusion was 14.1 +/- 2.7 and 14.4 +/- 2.1 [ml x (100 ml forearm)(-1) x min(-1)] in low and normal birth weight subjects, respectively. Insulin coinfusion increased acetylcholine-stimulated flow in both groups: 18.0 +/- 3.1 vs. 17.9 +/- 3.1 [ml x (100 ml forearm)(-1) x min(-1)], NS. Insulin infusion increased glucose uptake significantly in the normal birth weight group, compared with the low birth weight group: 0.40 +/- 0.09 to 1.00 +/- 0.16 vs. 0.44 +/- 0.09 to 0.59 +/- 0.1 [ micro mol glucose x (100 ml forearm)(-1) x min(-1)], P = 0.04. Young men with low birth weight have normal insulin-stimulated endothelial function and impaired insulin-stimulated forearm glucose uptake. Thus, endothelial dysfunction does not necessarily coexist with metabolic alterations in subjects with low birth weight.

Adipose Tissue↗

PubMed2004

Molecular mechanisms of impaired endothelial function associated with insulin resistance.

Dysfunction of the endothelium in large- and medium-sized arteries plays a central role in atherogenesis. The insulin resistance syndrome encompasses more than a subnormal response to insulin-mediated glucose disposal. Patients with this syndrome also frequently display elevated blood pressure, hyperlipidemia, and dysfibinolysis, even without any clinically manifested alteration in plasma glucose concentrations. Of note endothelial dysfunction and atherosclerosis also have been demonstrated in patients with hypertension, which is one of the features of the syndrome of insulin resistance. Insulin-induced vasodilation, which is mediated by the release of nitric oxide (NO) release, is impaired in obese individuals who display insulin resistance. Although it is tempting to speculate that loss of endothelium-dependent vasodilation and increased vasoconstriction might be etiological factors of elevated blood pressure, the factors contributing to NO-mediated endothelial dysfunction in the insulin-resistant state are not fully defined. Experimental evidences suggest that (6R)-5,6,7,8-tetrahydrobiopterin (BH(4)), the natural and essential cofactor of NO synthases (NOS), plays a crucial role not only in increasing the rate of NO generation by NOS but also in controlling the formation of superoxide anion (O(2)(-)) in the endothelial cells. Under insulin-resistant conditions where BH(4) levels are suboptimal, in addition to a reduced synthesis of NO, an accelerated inactivation of NO by O(2)(-) within the vascular wall was observed. Furthermore, oral supplementation of BH(4) restored endothelial function and relieved oxidative tissue damage, through activation of eNOS in the aorta of insulin-resistant rats. These results indicate that abnormal pteridine metabolism contributes to causing endothelial dysfunction and the enhancement of vascular oxidative stress in the insulin-resistant state.

Animals↗

PubMedDate not supplied

Endothelial function and hemodynamic responses during mental stress.

OBJECTIVE: The hemodynamic basis of blood pressure responses during psychological stress shows striking individual differences that share an interesting similarity with risk for cardiovascular disease. Factors accounting for these individual differences are poorly understood. The present study examined the relationship of vascular endothelial function to stress-induced hemodynamic responses. METHODS: Subjects were 40 healthy men and women, aged 25 to 44 years. Hemodynamic responses were assessed during exposure to a battery of four diverse laboratory stressors. Endothelium-dependent arterial dilation (EDAD) was measured by ultrasound imaging of the brachial artery in response to reactive hyperemia. RESULTS: High EDAD response was associated with lower resting systolic (p < .01) and diastolic blood pressure (p < .05). EDAD response was unrelated to blood pressure responses during stress. However, systemic vascular resistance responses during laboratory stress were significantly greater (p < .02) for individuals with low EDAD responses. CONCLUSIONS: Exaggerated systemic vascular resistance responses during stress may reflect endothelial dysfunction. This association may help explain the growing evidence of a relationship between stress hemodynamics and cardiovascular disease risk. The nature of this association is discussed in terms of a possible interplay between the sympathetic nervous system and the endothelium in regulation of vascular tone.

Adaptation, Psychological↗

PubMed2005

Impaired myocardial perfusion reserve but preserved peripheral endothelial function in patients with Fabry disease.

Fabry disease (McKusick 301500) is an X-linked lysosomal storage disorder due to deficient alpha-galactosidase A activity, which leads to accumulation of glycosphingolipids, especially in vascular smooth-muscle and endothelial cells. The effect of this accumulation on peripheral and cardiac vascular function is poorly known. We studied 15 Fabry patients (mean age 35 years and mean BMI 24.8 kg/m2) and 30 age- and BMI-matched healthy controls to examine whether myocardial perfusion reserve and peripheral artery endothelial function are altered. Myocardial perfusion was measured at rest and during dipyridamole-induced hyperaemia by positron emission tomography and H2(15)O. Myocardial blood flow reserve was calculated as the ratio between the dipyridamole-induced maximal blood flow and resting blood flow. Peripheral artery endothelial function was assessed by measuring the brachial artery flow-mediated dilatation using ultrasound at rest and during reactive hyperaemia. The myocardial perfusion reserve was significantly lower in Fabry patients than in controls (3.3+/-1.2 vs 4.4+/-1.6, p=0.02), while the brachial artery flow-mediated dilatation was similar (5.9%+/-3.9% vs 4.5%+/-3.6%, p=0.27). Thus, inFabry disease, myocardial perfusion reserve is reduced while the peripheral artery endothelial function is preserved.

Adult↗

PubMedDate not supplied

Redox modulation of insulin signaling and endothelial function.

Reactive oxygen and nitrogen species (ROS and RNS) recently emerged as critical signaling molecules in cardiovascular research. Several studies over the past decade have shown that physiological effects of vasoactive factors are mediated by these reactive species and, conversely, that altered redox mechanisms are implicated in the occurrence of metabolic and cardiovascular diseases. Oxidant stress occurs when ROS and/or RNS production exceeds the cell natural antioxidant systems, and pathological events ensue. Cardiovascular risk factors are associated with an imbalance of the redox equilibrium toward oxidative stress, leading to endothelial activation and proinflammatory processes implicated in atherogenesis and metabolic disorders. Recent studies indicate that insulin and insulin-sensitizing drugs activate antiinflammatory pathways that may limit oxidant stress in insulin target tissues. The main goal of this brief review is to discuss recent progress in the field of cellular redox signaling as it pertains to insulin modulation of vascular endothelial function in cardiovascular diseases.

Animals↗

PubMed1993

The effect of cholesterol reduction on the endothelial function and progression of atherosclerosis in WHHL rabbits.

In 3-month-old homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits the effect of treatment with the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor pravastatin was studied for 9 months and related to the endothelial function of the coronary arteries of isolated hearts and rings of the distal abdominal aorta. Oral administration of pravastatin in doses up to 40 mg/kg per day significantly decreased plasma cholesterol by 51% in comparison to untreated WHHL rabbits. Basal coronary flow and bradykinin-induced increase in coronary flow in Langendorff hearts of the pravastatin-treated animals were significantly greater than the flow in the control animals, whereas the metacholine-induced relaxation of abdominal aortic rings was not different and attenuated in comparison to New Zealand white rabbits. The incidence of atherosclerotic lesions in four main coronary arteries and the aorta was significantly lower in the pravastatin treated animals (25.0% and 52.8% respectively) than in untreated WHHL rabbits (34.1% and 80.0% respectively). The mean percentage of narrowing in the aorta was also significantly lower in the pravastatin-treated group (12.0%) than in the controls (25.2%). Significant correlations were found between the extent of atherosclerotic lesions and the bradykinin-induced increase in coronary flow versus plasma total cholesterol levels. Thus, in this model, long term cholesterol lowering treatment with pravastatin starting at an early age retards the progression of plaque formation and preserves the endothelium-dependent relaxation of the coronary arteries.

Animals↗

PubMed2004

Inhibition of oxidative stress and improvement of endothelial function by amlodipine in angiotensin II-infused rats.

BACKGROUND: Calcium channel blockers such as amlodipine are effective antihypertensive agents. In this study we investigated the effects of amlodipine on vascular oxidative stress, expression of the lectin-like oxidized low-density lipoprotein receptor (LOX-1), and endothelial function in angiotensin (Ang) II-infused rats. METHODS: Sprague-Dawley rats were treated with Ang II (0.7 mg/kg/day subcutaneously injected by mini-pump), with or without amlodipine (10 mg/kg/day by gavage), for 5 days and compared with control rats. Levels of aortic ring superoxide (O(2)(-)) and peroxynitrite (ONOO(-)) were determined, and systolic blood pressure (SBP) and endothelium-dependent relaxation were evaluated. RESULTS: Compared with control rats, Ang II-infused rats developed hypertension (175 +/- 3 v 135 +/- 2 mm Hg, P <.05), aortic hypertrophy (16.9 +/- 1.3 v 13.2 +/- 0.3 mg/cm, P <.05), left ventricular hypertrophy (0.236 +/- 0.003 v 0.204 +/- 0.004 g/100 g body weight, P <.05), and impaired endothelium-dependent relaxation (ED(50): 6.6 +/- 0.2 v 8.0 +/- 0.2 -log mol/L acetylcholine concentration, P <.05). Compared with control rats, Ang II-infused rats also had higher aortic levels of LOX-1 mRNA expression, O(2)(-)production (1005 +/- 140 v 608 +/- 159 counts/min/mg, P <.05), ONOO(-) production (1875 +/- 295 v 782 +/- 115 counts/min/mg, P <.05), and plasma free 8-F(2)alpha-isoprostanes (67.4 +/- 19.1 v 27.2 +/- 6.1 pg/mL, P <.05). In Ang II-infused rats SBP, aortic hypertrophy, endothelial dysfunction, LOX-1 expression, aortic O(2)(-) and ONOO(-) production, and plasma free 8-F(2)alpha-isoprostane levels were significantly reduced by amlodipine treatment. CONCLUSIONS: Amlodipine has antihypertensive and antioxidant activity in vivo, which effectively inhibits many of the oxidative stress-dependent mechanisms involved in Ang II-mediated cardiovascular injury.

Amlodipine↗

PubMed2003

Effect of short-term hormone therapy on oxidative stress and endothelial function in African American and Caucasian postmenopausal women.

In postmenopausal women (PMW), the effect of a short-term course of estrogen/progestin HT on free radical oxidative stress was evaluated. In addition, HT's effect on plasma nitric oxide (NO) activity was determined as a measure of vascular endothelial function. We investigated the relationship of these markers and HT across race and the cardiovascular risk factors of smoking, diabetes and hypertension.A prospective, observational study comparing preintervention and postintervention. Academic research center.Twenty-seven (14 African American and 13 Caucasian) PMW volunteers. Six weeks of continuous, combined estrogen/progestin HT. Plasma concentrations of free 8-epi-prostaglandin F(2alpha) (8-isoprostane) before and after HT were compared as a measure of oxidative stress. Nitrite, the stable oxidation metabolite of NO, was measured by the Greiss reaction after nitrate reduction to nitrite with cadmium. Plasma levels of free 8-isoprostane decreased significantly after 6 weeks of HT. Although almost all subjects benefited from the reduction in free 8-isoprostane, PMW with at least one cardiovascular risk factor (n = 19) demonstrated higher free 8-isoprostane than did subjects with no risk factors. Plasma levels of nitrite increased after 6 weeks of HT, but the difference was not statistically significant. Caucasian PMW demonstrated a greater increase in plasma levels of nitrite after 6 weeks of HT as compared with African American subjects, who exhibited almost no change.Short-term administration of HT significantly reduces oxidative stress in PMW and is consistent across race. However, there was an observed racial difference in endothelial NO response to HT between African American and Caucasian PMW.

Black People↗