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PubMed2006

Clinical assessment of endothelial dysfunction: combine and rule.

PURPOSE OF REVIEW: To briefly survey the literature for the past 2-3 years on the subject of diagnostic and prognostic markers of endothelial cell dysfunction. RECENT FINDINGS: Established and emerging techniques to detect endothelial cell dysfunction are divided into two large families: (1) functional and structural markers of endothelial cell dysfunction, and (2) surrogate markers of endothelial cell dysfunction. The first category includes high-resolution Doppler studies of conduit arteries, laser Doppler flowmetry of cutaneous microvasculature, and measurements of arterial stiffness and intima: media thickness. The second category of tests provides brief descriptions of detection of oxidative stress, inflammation, coagulation abnormalities, circulating endothelial cells and microparticles. I also focus on integration of various techniques and some novel genomic, proteomic and metabolomic tests. SUMMARY: This snapshot of existing and emerging technologies diagnosing endothelial cell dysfunction is intended to provide the foundation for the future (a) development of personalized noninvasive screening of endothelial function, and (b) delineation of preclinical diagnostic biomarkers heralding cardiovascular complications.

Biomarkers↗

PubMed1998

Early endothelial dysfunction in adults at risk from atherosclerosis: different responses to L-arginine.

OBJECTIVES: We sought to examine endothelial responses to L-arginine in three groups with isolated risk factors: hypercholesterolemia, smoking and insulin-dependent diabetes mellitus (IDDM). BACKGROUND: Endothelial dysfunction occurs early in atherosclerosis, predating clinical disease. We hypothesized that the nature of endothelial injury associated with individual cardiovascular risk factors might be different and that this might affect the response to L-arginine, the substrate for endothelial nitric oxide synthase. METHODS: We studied the effects of intravenous L-arginine on brachial artery flow-mediated dilation (FMD) and glyceryl trinitrate (GTN)-mediated dilation in 36 young subjects (18 to 40 years old) without clinical atherosclerosis: 9 each of normal control subjects, hypercholesterolemic subjects, cigarette smokers and subjects with IDDM. RESULTS: Baseline FMD was significantly impaired in hypercholesterolemic subjects (mean +/- SD 1.7 +/- 2.3%), smokers (1.6 +/- 1.8%) and diabetic subjects (1.8 +/- 1.5%) compared with that in control subjects (6.9 +/- 3.3%, p = 0.001). The response to GTN was not significantly different between the subjects with risk factors and control subjects, apart from those with IDDM, in whom it was significantly impaired (p = 0.026). After infusion of L-arginine, there was no change in FMD in control or diabetic subjects. In hypercholesterolemic subjects and smokers, FMD improved from 1.9 +/- 1.9% to 4.1 +/- 2.1% (p = 0.01) and from 2.0 +/- 1.71% to 3.1 +/- 2.5% (p = 0.02), respectively. CONCLUSIONS: FMD was impaired in all three risk factor groups; however, they responded differently to L-arginine, FMD being improved in hypercholesterolemic subjects and smokers but unchanged in diabetic subjects. These results indicate differing underlying pathophysiologies that may facilitate the design of treatment strategies for subjects with different risk factors.

Adolescent↗

PubMed2003

Treatment of glomerular endothelial dysfunction in steroid-resistant nephrosis with Ganoderma lucidum, vitamins C, E and vasodilators.

Glomerular endothelial dysfunction is believed to be responsible for the proteinuria and nephronal damage, namely tubulointerstitial fibrosis and glomerulosclerosis, observed in severe nephrosis such as focal segmental glomerulosclerosis. A dysfunctioning glomerular endothelium is likely to be induced by oxidative stress and oxidized LDL as well as altered immunocirculatory balance with a defective anti-inflammatory pathway. A defective release of vasodilator inconjunction with enhanced production of angiotensin II induces hemodynamic maladjustment by preferential constriction at the efferent arteriole. Such a hemodynamic maladjustment exerts two significant hemodynamic impacts. Close to the efferent constriction, it induces intraglomerular hypertension and glomerulosclerosis. Far from the efferent constriction, it reduces peritubular capillary flow, which eventually leads to tubulointerstitial fibrosis. Treatment with a vasodilator improves the hemodynamic maladjustment but does not completely suppress proteinuria. A successful suppression of proteinuria is accomplished by using Ganoderma lucidum and vitamins C and E. The beneficial effect of Ganoderma lucidum appears to be multifactorial, including the modulation of immunocirculatory balance, antilipid, vasodilator, antiplatelet and improved hemorheology. Together with vitamins C and E, this helps to neutralize oxidative stress and suppress the toxic effect to the glomerular endothelial function.

Adrenal Cortex Hormones↗

PubMed2002

Exercise training and endothelial dysfunction in coronary artery disease and chronic heart failure. From molecular biology to clinical benefits.

Endothelial dysfunction (ED) has been documented in patients with both coronary artery disease (CAD) and chronic heart failure (CHF)-being responsible for exercise-induced myocardial ischemia in the former and increased afterload in the latter. In the last two decades exercise training has assumed a major role in both cardiovascular disorders. In CAD exercise training has established positive effects on myocardial perfusion. Recently, exercise training has been shown to attenuate paradoxical vasoconstriction in CAD. The improved ED after training explains the improvement of myocardial perfusion in the absence of changes in baseline coronary artery diameter. Since ED has been identified as a predictor of coronary events exercise may contribute to long-term reductions of cardiovascular mortality. In CHF the increased peripheral vascular resistance - especially during exercise - is more important. ED contributes to the peripheral vasoconstriction. Training programs have shown to improve ED in CHF. A long-term study of hemodynamic effects of training in CHF revealed a significant reduction of total peripheral resistance (TPR) that after 6 months with a concomitant increase in stroke volume. In a subgroup analysis a significant correlation between changes in TPR and changes in peripheral ED was observed. Cell culture and animal experiments suggest that shear stress increases the endothelial L-arginine uptake, enhances NO synthase activity and expression, and upregulates the production of extracellular superoxide dismutase, which prevents premature NO breakdown. All these molecular effects converge on a reduction of myocardial ischemic events in CAD and a decrease of afterload in CHF.

Chronic Disease↗

PubMed1998

Endothelial dysfunction in hypertension: fact or fancy?

Endothelium can deeply influence vascular tone and structure. The main endothelium-derived factor is nitric oxide (NO), which not only is a potent vasodilator but also inhibits platelet aggregation, smooth muscle cell proliferation, monocyte adhesion, and adhesion molecule expression, thus protecting the vessel wall against the development of atherosclerosis and thrombosis. In human hypertension, endothelial dysfunction has been documented in peripheral and coronary macro- and microcirculation and in renal circulation. Impaired endothelium-dependent vasodilatation associated with essential hypertension appears to be a primary phenomenon because it can be detected in the offspring of essential hypertensive patients, shows no clear correlation with blood pressure value, and is not normalized by the mere reduction of blood pressure. The phenomenon responsible for endothelial alteration in essential hypertensive patients appears to be the activation of an alternative pathway involving cyclo-oxygenase (COX), which reduces NO availability through production of oxidative stress. This alteration in the NO pathway could be the main mechanism through which a dysfunctional endothelium may promote atherosclerosis and thrombosis in essential hypertension. Therefore, an important aim of antihypertensive therapy would be not only to normalize blood pressure values but also to reverse endothelial dysfunction by restoring NO availability. Evidence indicates that different classes of antihypertensive compounds have different effects on this alteration. Dihydropiridine calcium antagonists appear to act specifically on the NO pathway by a mechanism that is probably related to antioxidant activity.

Endothelium, Vascular↗

PubMed2000

An association between microvascular endothelial dysfunction, transcardiac nitric oxide production and pro-inflammatory cytokines after heart transplantation in humans.

Endothelial dysfunction anticipates the development of transplant coronary artery disease (TxCAD) observed more than 1 year after transplantation (HTx). We investigated whether in patients early after HTx myocardial inducible and constitutive nitric oxide synthases (iNOS; cNOS) are expressed and cardiac nitric oxide production occurs. Moreover, a possible relationship to alterations in endothelium dependent and independent vasomotor function was assessed. Forty-two transplant recipients were studied 37 +/- 5 days after HTx. Microvascular coronary flow velocity reserve (CFVR) was tested endothelium dependent (acetylcholine; 30 microg/min x 5 min/i.c.) and independent (adenosine; 160 microg/min x 5 min/i.c.) by Doppler flow wire. Flow velocity increase by a factor greater than 2 was considered normal. Quantitative coronary angiography was used to assess epicardial vasomotor function in response to the same stimuli. Myocardial iNOS and cNOS gene expression were detected by semiquantitative reversed transcriptase polymerase chain reaction. Plasma nitrite levels (microM) were measured by spectrophotometry. Cytokines (TNF-alpha, IL-6; pg/ml) were measured by enzyme linked immunosorbent assay. In 26.1% of patients (n = 11; group A) an impaired endothelium dependent CFVR (1.65 +/- 0.23 increase) was observed; in 73.9% (n = 31, group B) a normal endothelium dependent CFVR (3.0 +/- 0.7 increase; P = 0.003) was observed. Myocardial iNOS and cNOS gene expression did not differ between the two groups. Transcardiac cytokine production was noted in 58.8% of patients for IL-6 and in 53.3% for TNF-alpha. Coronary sinus (CS) levels of TNF-alpha, IL-6 and nitrite were higher in group A. A significant increase in nitrite production was found only in patients with impaired endothelium dependent CFVR (aorta: 43.9 +/- 3.7 vs CS: 52.8 +/- 5.6, P = 0.05), suggesting transcardiac nitric oxide production. In addition, CS nitrite levels correlated with CS TNF-alpha levels in patients with impaired CFVR (r = 0.44, P = 0.003). Microvascular endothelium dependent CFVR is impaired in 26% of patients early after HTx. Activation of cytokines and the NO pathway seem to be involved in this vasomotor dysfunction The association between cardiac nitric oxide production and TNF-alpha in this group indicates a chronic high immunologic process, which may represent an early and important target for therapy and prevention of TxCAD.

Adenosine↗

PubMed2005

Inhaled but not intravenous milrinone prevents pulmonary endothelial dysfunction after cardiopulmonary bypass.

OBJECTIVE: Cardiopulmonary bypass triggers a systemic inflammatory response that alters pulmonary endothelial function, which can contribute to pulmonary hypertension. Milrinone is a type III phosphodiesterase inhibitor. The objective of this study was to compare the effects of inhaled and intravenous milrinone on the pulmonary endothelium-dependent relaxations and hemodynamic and oxygenation parameters after cardiopulmonary bypass in a porcine model. METHODS: Five groups of Landrace swine were compared: (1) control group, no cardiopulmonary bypass; (2) bypass group, 90 minutes of normothermic bypass and 60 minutes of reperfusion; (3) inhaled milrinone group, bypass preceded by a 1.8-mg bolus of inhaled milrinone followed by a continuous milrinone nebulization; (4) intravenous milrinone group, bypass preceded by 2 mg of intravenous milrinone; and (5) inhaled NaCl group, bypass preceded by inhaled saline solution. After sacrifice, pulmonary arterial endothelium-dependent relaxations to acetylcholine and bradykinin were studied in organ chambers. RESULTS: Inhaled milrinone caused less hypotension ( P < .05), a lesser decrease in peripheral vascular resistances ( P < .01), and a lower heart rate ( P < .05) than intravenous milrinone. Inhaled milrinone prevented the alterations in relaxations of pulmonary arteries to acetylcholine caused by cardiopulmonary bypass, and relaxations to bradykinin were improved in the inhaled milrinone group ( P < .05) compared with the cardiopulmonary bypass and control groups. CONCLUSIONS: Inhaled milrinone prevents the occurrence of the pulmonary endothelial dysfunction seen after cardiopulmonary bypass. The hemodynamic and oxygenation profiles obtained with inhaled milrinone are safer than with intravenous milrinone. These strategies might be useful in preventing pulmonary hypertension after cardiac surgery.

Acetylcholine↗

PubMed2002

Chronic ET(A) receptor blockade prevents endothelial dysfunction of small arteries in apolipoprotein E-deficient mice.

OBJECTIVE: This study investigated whether endothelial dysfunction occurs in mesenteric arteries of apoE-deficient mice and determined the role of endothelin (ET)-1, which is increased in human atherosclerosis, using an orally active endothelin ET(A) receptor antagonist. METHODS: ApoE-deficient and C57BL/6J control mice were fed for 30 weeks with normal chow or high-fat Western-type diet alone or in combination with darusentan (LU135252; 50 mg/kg/day). Vasomotor reactivity of isolated small mesenteric arteries (I.D. 200-250 microm) was studied in vitro under perfused and pressurized conditions. RESULTS: In both mouse strains, about one fourth of the endothelium-dependent relaxant response to acetylcholine was insensitive to inhibition by L-NAME and indomethacin. In mesenteric arteries of apoE-deficient mice on Western-type diet, increased intima-media thickness and levels of endothelin-1 protein were observed. In addition, NO-mediated endothelium-dependent relaxation to acetylcholine was reduced without affecting L-NAME/indomethacin insensitive relaxation and contractions to endothelin-1 and serotonin were enhanced. Treatment with darusentan normalized vascular structure, NO-mediated relaxation to acetylcholine and contractions to endothelin-1 and serotonin without affecting blood pressure or plasma cholesterol levels. CONCLUSIONS: Severe hypercholesterolemia in apoE-deficient mice is associated with attenuation of NO-mediated relaxation to acetylcholine and increased vascular endothelin-1 content. Chronic ET(A) receptor blockade may provide a new therapeutic approach to improve NO-mediated endothelium-dependent vasomotion in small arteries.

Acetylcholine↗

PubMed1996

Endothelial dysfunction in hypertension.

PURPOSE: To summarize how abnormal release of relaxing and contracting factors from endothelial cells contribute to the vascular abnormalities in hypertension. ENDOTHELIUM-DERIVED FACTORS: The endothelium controls the tone of the underlying vascular smooth muscle by releasing relaxing and contracting factors. The former include prostacyclin, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), and the latter endoperoxides, thromboxane A2, superoxide anions and endothelin. HYPERTENSION: In most types of hypertension, endothelium-dependent relaxations are curtailed, because of a reduced production and/or action of endothelium-derived NO and EDHF. In essential hypertension, endothelium-dependent relaxations are reduced also because of the endothelium-dependent production of vasoconstrictor prostanoids (endoperoxides and, in some cases, thromboxane A2). CAUSE OR CONSEQUENCE: The endothelial dysfunction observed in hypertensive blood vessels is likely to be a consequence rather than a cause of the disease process. THERAPEUTIC IMPLICATIONS: Enhanced release of endothelium-derived relaxing factors (NO and EDHF) help to explain the therapeutic effects of inhibitors of converting enzyme.

Animals↗

PubMed2003

Vasopeptidase inhibition: a new treatment approach for endothelial dysfunction.

Angiotensin-converting enzyme (ACE) inhibition is a well-established principle in the treatment of endothelial dysfunction. Numerous preclinical and clinical studies have clearly demonstrated the beneficial effects of inhibiting the renin-angiotensin-aldosterone system (RAS) in states of impaired endothelial function. The successful use of ACE inhibitors encouraged attempts to inhibit other key enzymes in the regulation of vascular tone, such as the neutral endopeptidase (NEP). Similar to ACE, NEP is an endothelial cell surface metalloproteinase that is involved in the degradation of several regulatory peptides, including the natriuretic peptides, and, thus, NEP inhibition augments vasodilatation and natriuresis through increased levels of atrial natriuretic peptide (ANP). By inhibiting the RAS and potentiating the natriuretic peptide system at the same time, combined NEP/ACE inhibitors, the so-called vasopeptidase inhibitors, reduce vasoconstriction and enhance vasodilatation, thereby decreasing peripheral vascular resistance and blood pressure. Within the vessel wall this may lead to a reduction of vasoconstrictor and proliferative mediators, such as angiotensin II and endothelin-1, and may increase local levels of bradykinin as well as natriuretic peptides. Even though first results of both preclinical and clinical studies indicate that combined inhibition of ACE and NEP by vasopeptidase inhibitors represents a promising strategy in the treatment of hypertension and heart failure, angioedema occurs more frequently on vasopeptidase inhibition as compared to ACE inhibition. To establish vasopeptidase inhibition as a novel option in the treatment of cardiovascular disease, further validation of efficacy and safety of this promising therapeutic principle is mandatory.

Animals↗

PubMed1988

Split-dose sparing of gamma-ray-induced pulmonary endothelial dysfunction in rats.

The purpose of this study was to determine whether radiation-induced pulmonary endothelial dysfunction exhibits split-dose sparing. Rats were sacrificed 2 months after a range of 60Co gamma-ray doses (0-40 Gy) delivered to the right hemithorax in either a single fraction or in two equal fractions separated by 24 h. Pulmonary angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin (PGI2) and thromboxane (TXA2) production served as indices of lung endothelial function. There were dose-dependent decreases in ACE and PLA activity and increases in PGI2 and TXA2 production after both single and split-dose exposures. The D2-D1 values determined from the two-fraction minus single-fraction isoeffective doses were 3.9 Gy for ACE activity, 7.2 Gy for PLA activity, 4.8 Gy for PGI2 production, and 4.7 Gy for TXA2 production. Thus these data demonstrate that over the present range of radiation doses approximately 4-7 Gy is repairable as subeffective endothelial damage during the 24-h interval between fractions. These values agree with previously published estimates of split-dose sparing in mouse lung based on lethality and breathing rate assays.

Animals↗

PubMedDate not supplied

Endothelial dysfunction in chronic kidney disease: determinant of susceptibility to end-organ damage and therapeutic response.

Endothelial dysfunction (ED) seems to be a crucial mediator of increased cardiovascular risk observed among patients with chronic kidney disease (CKD). Importantly, systemic ED does not only occur in patients with severe renal failure, but also in individuals with earlier stages of CKD. Close association between microalbuminuria and systemic ED renders renal vascular function an important marker for the severity of cardiovascular damage. Furthermore, changes in renal endothelium might be actively involved in the progression of renal end-organ damage. Recently, experimental evidence showed that interindividual variability in endothelial function of healthy rats predicts susceptibility to renal damage and the efficacy of renoprotective treatment. Therefore, a specific manipulation of renal and systemic ED might provide benefits in various stages of CKD. ED thus may represent an ideal therapeutic target not only for treatment, but also for primary prevention of renal disease.

Cardiovascular Diseases↗

PubMed2001

Plasma markers of endothelial dysfunction in chronic obstructive pulmonary disease.

We studied some endothelial cell activity plasma markers, nitric oxide (NO), thrombomodulin (TM), selectins (sP-, sE-, sL-selectin: platelet-P, endothelium-E, leukocyte-L), and tissue factor pathway inhibitor (TFPI) in 14 patients with chronic obstructive pulmonary disease (COPD), matched with 20 normal controls, to evaluate their endothelial cell dysfunction. Both NO (patients: 23.42 +/- 1.67 microg/mL: controls: 40.0 +/- 3.38 microg/mL) and TM levels (patients: 5.46 +/- 1.32 ng/mL; controls: 12.9 +/- 0.51 ng/mL) were significantly decreased in COPD (p < 0.001). sP-selectin levels (patients: 79.42 +/- 18.20 ng/mL, controls: 37.5 +/- 2.84 mg/mL) were significantly higher (p < 0.02), whereas sL-selectin levels (patients: 584.9 +/- 78.98 ng/mL, controls: 1,054.02 +/- 61.28 ng/mL) were significantly decreased in patients with COPD (p < 0.001). In contrast, no differences were seen in sE-selectin. Patients with COPD showed a significantly higher (p < 0.001) TFPI antigen plasma level (mean 112.28 +/- 6 .45 ng/mL; controls 77.68 +/- 0.28 ng/mL) than controls. Our data support the concept of some form of endothelial cell dysfunction, and coagulation abnormalities are present in patients with COPD. However, because the endothelium seems to produce a defense mechanism, the potential usefulness of an antithrombotic therapy in these patients needs further investigation.

Aged↗

PubMed2006

[The role of endothelial dysfunction in the pathogenesis of combined cardiopulmonary diseases].

The aim of the study was to evaluate the endothelial function in patients with coronary heart disease and an exacerbation of chronic obstructive pulmonary disease (COPD), and the role of endothelial dysfunction (ED) in the pathogenesis of reciprocal exacerbation syndrome in cases of combined cardiovascular pathology. The subjects were 366 patients with single or combined cardiovascular diseases, in whom non-invasive evaluation of the endothelial regulation of the vascular tone was performed, and serum levels of NO were measured. The study revealed the biggest number of cases with an altered endothelium-dependent vasodilatation, and the most prominent decrease in NO level in patients with CHD and COPD. All the patients were followed up during two years in order to compare clinical manifestations of single and combined cardiovascular pathology. The results show that ED may be considered a predictor of complicated clinical course of COPD in patients with CHD.

Comorbidity↗

PubMed2006

[Resistive exercise in the evaluation of endothelial dysfunction in heart failure].

OBJECTIVE: To evaluate the use of resistive exercise in the study of endothelial dysfunction in heart failure (HF) comparatively to reactive hyperemia (RH). METHODS: Eighteen patients with heart failure and 15 normal volunteers were submitted to intermittent handgrip exercise in a pneumatic bag, at an intensity that corresponds to 75% of the previously assessed maximum load. Patients underwent high-resolution vascular ultrasonography for brachial artery diameter and flow evaluation as well as cardiac output determination at rest, RH and after exercise. The systolic flow index in the brachial artery and cardiac index were calculated. RESULTS: Systolic flow index increase in the brachial artery was observed after RH and physical exercise, with the latter presenting the highest increase. There was an increase in the cardiac index after the study conditions in comparison to resting conditions. CONCLUSION: Resistive exercise, performed at the assessed load, increases blood flow more intensively than RH, constituting a physiological option for the evaluation of endothelial function in HF.

Adolescent↗

PubMed2005

Metabolic syndrome, endothelial dysfunction, and erectile dysfunction: association and management.

The metabolic syndrome, the criteria for which include glucose intolerance, obesity, hypertension, and dyslipidemia, has rapidly become understood to have a major association with erectile dysfunction (ED). On a mechanistic level, their common grounds may involve endothelial dysfunction, although the conditions of oxidative stress understood to be a pathologic element of the syndrome also may affect various components of the vascular biology of the penis. The foremost importance of recognizing the association between ED and the metabolic syndrome is that addressing ED presentations may afford opportunities to identify and improve a major adverse health profile and thereby promote health maintenance objectives for patients.

Endothelium, Vascular↗

PubMed2004

Endothelial dysfunction, atherosclerosis and thrombosis in uremia--possibilities of intervention.

Chronic renal failure is a state of prominent endothelial dysfunction, accelerated atherosclerosis, high incidence of thromboembolic complications and excess cardiovascular mortality. We reviewed up-to-date experimental and clinical data showing close and deleterious links between these entities. Emerging therapeutic interventions aimed at improvement of endothelial function and better clinical outcomes in chronic kidney disease patients were also discussed.

Animals↗

PubMed2006

Soy protein diet improves endothelial dysfunction in renal transplant patients.

BACKGROUND: Since it has been demonstrated that soy diet can improve endothelial function, in the present study we evaluated the effect of dietary substitution of 25 g of animal proteins with soy proteins on endothelial dysfunction in renal transplant patients. METHODS: In 20 renal transplant patients (55 +/- 11 years, serum creatinine 1.7 +/- 0.6 mg/dl), brachial artery flow mediated dilation (FMD) and endothelium-independent vasodilation (sublingual nitroglycerine, 25 microg) were measured at baseline, after 5 weeks of a soy diet and finally after 5 weeks of soy wash-out. Changes in plasma lipids, markers of oxidative stress (lipid peroxides, LOOH) and inflammation (C-reactive protein), isoflavones (genistein and daidzein), asymmetric dimethyl arginine (ADMA) and L-arginine were also evaluated. RESULTS: At baseline, patients showed a significantly lower FMD as compared with age-matched healthy subjects (3.2 +/- 1.8 vs 6.3 +/- 1.9, respectively; P < 0.001), while response to nitroglycerine was similar. After soy diet, actual protein intake was not changed, cholesterol and lipid peroxides were significantly reduced, and isoflavones were detectable in plasma. Soy diet was associated with a significant improvement in FMD (4.4 +/- 2.0; P = 0.003 vs baseline), while response to nitroglycerine was unchanged. Improvement in FMD was related to L-arginine/ADMA ratio changes, but no significant relation was found to changes in cholesterol, lipid peroxides or genistein and daidzein plasma concentrations. After 5 weeks of soy diet discontinuation, FMD (3.3 +/- 1.7%) returned to baseline values and isoflavones were no longer detectable in plasma. CONCLUSIONS: A soy protein diet for 5 weeks improves endothelial function in renal transplant patients. This effect seems to be strictly dependent on soy intake as it disappears after soy withdrawal and is mediated by an increase in the L-arginine/ADMA ratio, independently of change in lipid profile, oxidative stress or isoflavones.

Adult↗