Dual sEH/COX-2 Inhibition Using PTUPB—A Promising Approach to Antiangiogenesis-Induced Nephrotoxicity

Kidney injury from antiangiogenic chemotherapy is a significant clinical challenge, and we currently lack the ability to effectively treat it with pharmacological agents. Thus, we set out to investigate whether simultaneous soluble epoxide hydrolase (sEH) and cyclooxygenase-2 (COX-2) inhibition using a dual sEH/COX-2 inhibitor PTUPB could be an effective strategy for treating antiangiogenic therapy-induced kidney damage. We used a multikinase inhibitor, sorafenib, which is known to cause serious renal side effects. The drug was administered to male Sprague–Dawley rats that were on a high-salt diet. Sorafenib was administered over the course of 56 days. The study included three experimental groups; 1) control group (naïve rats), 2) sorafenib group [rats treated with sorafenib only (20 mg/kg/day p.o.)], and 3) sorafenib + PTUPB group (rats treated with sorafenib only for the initial 28 days and subsequently coadministered PTUPB (10 mg/kg/day i.p.) from days 28 through 56). Blood pressure was measured every 2 weeks. After 28 days, sorafenib-treated rats developed hypertension (161 ± 4 mmHg). Over the remainder of the study, sorafenib treatment resulted in a further elevation in blood pressure through day 56 (200 ± 7 mmHg). PTUPB treatment attenuated the sorafenib-induced blood pressure elevation and by day 56, blood pressure was 159 ± 4 mmHg. Urine was collected every 2 weeks for biochemical analysis. After 28 days, sorafenib rats developed pronounced proteinuria (9.7 ± 0.2 P/C), which intensified significantly (35.8 ± 3.5 P/C) by the end of day 56 compared with control (2.6 ± 0.4 P/C). PTUPB mitigated sorafenib-induced proteinuria, and by day 56, it reduced proteinuria by 73%. Plasma and kidney tissues were collected on day 56. Kidney histopathology revealed intratubular cast formation, interstitial fibrosis, glomerular injury, and glomerular nephrin loss at day 56 in sorafenib-treated rats. PTUPB treatment reduced histological features by 30%–70% compared with the sorafenib-treated group and restored glomerular nephrin levels. Furthermore, PTUPB also acted on the glomerular permeability barrier by decreasing angiotensin-II-induced glomerular permeability to albumin. Finally, PTUPB improved in vitro the viability of human mesangial cells. Collectively, our data demonstrate the potential of using PTUPB or dual sEH/COX-2 inhibition as a therapeutic strategy against sorafenib-induced glomerular nephrotoxicity.

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Evidence for Peripheral Vascular Involvement in Mild Elevation of Blood Pressure in Man

Clinical Science ◽

10.1042/cs051065s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 65s-68s

Author(s):

R. Sivertsson ◽

R. Sannerstedt ◽

Y. Lundgren

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cardiac Index ◽

Structural Changes ◽

Vascular Involvement ◽

Control Group ◽

Study Group ◽

Blood Pressure Elevation ◽

Pressure Elevation ◽

Arterial Blood

1. Cardiac output at rest, intra-arterial blood pressure and hand blood flow at maximal vasodilatation were studied in two groups of 18–25-year-old men: forty-four with mild blood pressure elevation were referred from a military enlistment centre, and twenty-nine normotensive volunteers were mainly recruited from the same enlistment centre. 2. The study group was characterized by a significantly higher cardiac index at rest, and a significantly higher blood flow resistance in the hand at maximal vasodilatation than the control group, indicating the presence of structural modifications in the resistance vessels of patients with mild blood pressure elevation. 3. The tendency to increased vascular resistance in the blood vessels of the hand at maximal vasodilatation was more pronounced in patients with a normal cardiac index than in those with a high index. This suggests inclusion in the study group of tense, anxious individuals with an elevated cardiac index but otherwise normal circulation, but does not exclude the possibility that these patients may develop structural changes later on.

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Risk factors and AGTR1 gene polymorphism (1166A>C) in patients with essential hypertension

Bukovinian Medical Herald ◽

10.24061/2413-0737.xxiv.4.96.2020.109 ◽

2020 ◽

Vol 24 (4 (96)) ◽

pp. 99-104

Author(s):

M. Semianiv

Keyword(s):

Risk Factors ◽

Blood Pressure ◽

Body Mass Index ◽

Essential Hypertension ◽

Diastolic Blood Pressure ◽

Body Mass ◽

Control Group ◽

Blood Pressure Elevation ◽

A1166c Polymorphism ◽

Gender And Age

Objective – to analyze the association of risk factors with the 1666 A>C polymorphism of the AGTR1 gene in patients with essential hypertension.Material and methods. 100 patients were screened, 72 of whom were genotyped. The control group consisted of 48 healthy individuals who did not differ in gender and age, and with the group of patients.Results. The obtained data confirmed that the level of blood pressure elevation is associated, to some extent, with modified (diabetes mellitus 2, smoking, body mass index) and unmodified factors (family history, gender) the risk of essential hypertension. The results of the analysis of blood pressure levels considering the A1166C polymorphism of the AGTR1 gene showed that the values of systolic and diastolic blood pressure in the group of patients with C-allele carriers were higher than in carriers of AA genotype: SBP – by 5.38% (p<0.05), DBP – by 5.15% (p<0.05). Conclusions. The level of blood pressure in patients with essential hypertension depends on body mass index and smoking. In carriers of the C-allele of the AGTR1 gene (A1166C), the level of systolic and diastolic blood pressure exceeds the ones of the carriers of the AA genotype. The presence of the C-allele of the AGTR1 gene (A1166C) almost doubles the risk of severe essential hypertension [OR = 2.75; p = 0.037].

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P0984SGLT2 INHIBITION PREVENTS RENAL FIBROSIS IN CYCLOSPORINE NEPHROPATHY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0984 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Giovanna Castoldi ◽

Raffaella Carletti ◽

Silvia Ippolito ◽

Massimiliano Colzani ◽

Francesca Barzaghi ◽

...

Keyword(s):

Blood Pressure ◽

Diabetic Nephropathy ◽

Tyrosine Hydroxylase ◽

Renal Fibrosis ◽

Interstitial Fibrosis ◽

Control Group ◽

Diabetic Patients ◽

Protective Effects ◽

Type 2 Diabetic Patients ◽

Inflammatory Infiltrates

Abstract Background and Aims Sodium glucose cotransporter 2 (SGLT2) inhibitors, a new class of antidiabetic drugs, showed nephroprotection in type 2 diabetic patients. The mechanisms underlying nephroprotection are not completely known and it is unclear whether the nephroprotective effects are present also in non-diabetic nephropathy. The aim of this study was to evaluate the effects of empagliflozin, a SGLT-2 inhibitor, in cyclosporine nephropathy in the absence of diabetes. Method Ten days before the beginning and then during the entire experimental periods, low-salt diet (Teklad 7034) was administered to Sprague Dawley rats. Cyclosporine-A (CsA, 15 mg/kg/day, intraperitoneal injection; n=6) and CsA plus empagliflozin (Empa, 10 mg/kg /day, per os; n=6) were administered for 4 weeks. Control group was treated with placebo (n=6). Blood pressure was measured by plethysmographic method at the beginning and at the end of the experimental period. At the end of the protocol, the kidneys were excised for histomorphometric analysis of renal fibrosis and for immunohistochemical evaluation of inflammatory infiltrates and tyrosine hydroxylase expression, used as marker of symphatetic nerve activity. Results The rats treated with CsA showed a significant increase (p <0.01) in blood pressure, which was slightly reduced by administration of empagliflozin. CsA administration caused an increase in glomerular and tubulo-interstitial fibrosis (p <0.05), renal inflammatory infiltrates (p <0.05) and tyrosine hydroxylase expression (p <0.01) as compared to the control rats. Treatment with empagliflozin reduced glomerular and tubulo-interstitial fibrosis (p <0.05), inflammatory cell infiltration (p <0.01) and tyrosine hydroxylase expression (p <0.01), as compared to CsA-treated rats. Conclusion Empagliflozin administration showed protective effects on cyclosporine nephropathy, decreasing renal fibrosis, macrophage infiltration and tyrosine hydroxylase expression. These data suggest that the nephroprotective role of empagliflozin could not be restricted only to diabetic nephropathy.

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Virgin Coconut Oil Prevents Blood Pressure Elevation and Improves Endothelial Functions in Rats Fed with Repeatedly Heated Palm Oil

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/629329 ◽

2013 ◽

Vol 2013 ◽

pp. 1-7 ◽

Cited By ~ 20

Author(s):

Badlishah Sham Nurul-Iman ◽

Yusof Kamisah ◽

Kamsiah Jaarin ◽

Hj Mohd Saad Qodriyah

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Palm Oil ◽

Coconut Oil ◽

Male Rats ◽

Control Group ◽

Virgin Coconut Oil ◽

Blood Pressure Elevation ◽

Pressure Elevation ◽

Endothelial Functions

This study was performed to explore the effects of virgin coconut oil (VCO) in male rats that were fed with repeatedly heated palm oil on blood pressure, plasma nitric oxide level, and vascular reactivity. Thirty-two male Sprague-Dawley rats were divided into four groups: (i) control (basal diet), (ii) VCO (1.42 mL/kg, oral), (iii) five-times-heated palm oil (15%) (5HPO), and (iv) five-times-heated palm oil (15%) and VCO (1.42 mL/kg, oral) (5HPO + VCO). Blood pressure was significantly increased in the group that was given the 5HPO diet compared to the control group. Blood pressure in the 5HPO + VCO group was significantly lower than the 5HPO group. Plasma nitric oxide (NO) level in the 5HPO group was significantly lower compared to the control group, whereas in the 5HPO + VCO group, the plasma NO level was significantly higher compared to the 5HPO group. Aortic rings from the 5HPO group exhibited attenuated relaxation in response to acetylcholine and sodium nitroprusside as well as increased vasoconstriction to phenylephrine compared to the control group. Aortic rings from the 5HPO + VCO group showed only attenuated vasoconstriction to phenylephrine compared to the 5HPO group. In conclusion, VCO prevents blood pressure elevation and improves endothelial functions in rats fed with repeatedly heated palm oil.

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Lymphocyte responses exacerbate angiotensin II-dependent hypertension

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00373.2009 ◽

2010 ◽

Vol 298 (4) ◽

pp. R1089-R1097 ◽

Cited By ~ 144

Author(s):

Steven D. Crowley ◽

Young-Soo Song ◽

Eugene E. Lin ◽

Robert Griffiths ◽

Hyung-Suk Kim ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Sodium Excretion ◽

Kidney Injury ◽

Scid Mice ◽

Prostaglandin E ◽

Ang Ii ◽

Blood Pressure Elevation ◽

Cox 2 ◽

Lymphocyte Responses

Activation of the immune system by ANG II contributes to the pathogenesis of hypertension, and pharmacological suppression of lymphocyte responses can ameliorate hypertensive end-organ damage. Therefore, to examine the mechanisms through which lymphocytes mediate blood pressure elevation, we studied ANG II-dependent hypertension in scid mice lacking lymphocyte responses and wild-type controls. Scid mice had a blunted hypertensive response to chronic ANG II infusion and accordingly developed less cardiac hypertrophy. Moreover, lymphocyte deficiency led to significant reductions in heart and kidney injury following 4 wk of angiotensin. The muted hypertensive response in the scid mice was associated with increased sodium excretion, urine volumes, and weight loss beginning on day 5 of angiotensin infusion. To explore the mechanisms underlying alterations in blood pressure and renal sodium handling, we measured gene expression for vasoactive mediators in the kidney after 4 wk of ANG II administration. Scid mice and controls had similar renal expression for interferon-γ, interleukin-1β, and interleukin-6. By contrast, lymphocyte deficiency (i.e., scid mice) during ANG II infusion led to upregulation of tumor necrosis factor-α, endothelial nitric oxide synthase (eNOS), and cyclooxygenase-2 (COX-2) in the kidney. In turn, this enhanced eNOS and COX-2 expression in the scid kidneys was associated with exaggerated renal generation of nitric oxide, prostaglandin E2, and prostacyclin, all of which promote natriuresis. Thus, the absence of lymphocyte activity protects from hypertension by allowing blood pressure-induced sodium excretion, possibly via stimulation of eNOS- and COX-2-dependent pathways.

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Relation between Perioperative Hypertension and Intracranial Hemorrhage after Craniotomy

Anesthesiology ◽

10.1097/00000542-200007000-00012 ◽

2000 ◽

Vol 93 (1) ◽

pp. 48-54 ◽

Cited By ~ 165

Author(s):

Ayman Basali ◽

Edward J. Mascha ◽

Iain Kalfas ◽

Armin Schubert

Keyword(s):

Blood Pressure ◽

Hospital Stay ◽

Intracranial Hemorrhage ◽

Systemic Hypertension ◽

Control Group ◽

Inclusion Criteria ◽

Control Groups ◽

Retrospective Case ◽

Blood Pressure Elevation ◽

Prolonged Hospital

Background Previous data suggest that systemic hypertension (HTN) is a risk factor for postcraniotomy intracranial hemorrhage (ICH). The authors examined the relation between perioperative blood pressure elevation and postoperative ICH using a retrospective case control design. Methods The hospital's database of all patients undergoing craniotomy from 1976 to 1992 was screened. Coagulopathic and unmatchable patients were excluded. There were 69 evaluable patients who developed ICH postoperatively (n = 69). A 2-to-1 matched (by age, date of surgery, pathologic diagnosis, surgical procedure, and surgeon) control group without postoperative ICH was assembled (n = 138). Preoperative, intraoperative, and postoperative blood pressure records (up to 12 h) were examined. Incidence of perioperative HTN (blood pressure > or = 160/90 mmHg) and odds ratios for ICH were determined. Results Of the 11,214 craniotomy patients, 86 (0.77%) suffered ICH, and 69 fulfilled inclusion criteria. The incidence of preoperative HTN was similar in the ICH (34%) and the control (24%) groups. ICH occurred 21 h (median) postoperatively, with an interquartile range of 4-52 h. Sixty-two percent of ICH patients had intraoperative HTN, compared with only 34% of controls (P < 0.001). Sixty-two percent of the ICH patients had prehemorrhage HTN in the initial 12 postoperative hours versus 25% of controls (P < 0.001), with an odds ratio of 4.6 (P < 0.001) for postoperative ICH. Hospital stay (median, 24.5 vs. 11.0 days), and mortality (18.2 vs. 1.6%) were significantly greater in the ICH than in the control groups. Conclusions ICH after craniotomy is associated with severely prolonged hospital stay and mortality. Acute blood pressure elevations occur frequently prior to postcraniotomy ICH. Patients who develop postcraniotomy ICH are more likely to be hypertensive in the intraoperative and early postoperative periods.

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The cytochrome 11B2 aldosterone synthase gene CYP11B2 (RS1799998) polymorphism associates with chronic kidney disease in hypertensive patients

Biointerface Research in Applied Chemistry ◽

10.33263/briac103.406411 ◽

2020 ◽

Vol 10 (3) ◽

pp. 5406-5411 ◽

Cited By ~ 2

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Serum Levels ◽

Control Group ◽

Allelic Polymorphism ◽

Blood Pressure Elevation ◽

Aldosterone Synthase ◽

Hypertensive Population ◽

Increased Risk

Renin-angiotensin aldosterone system (RAAS) holds a crucial role in blood pressure regulation. Aldosterone is encoded by the cytochrome 11B2 aldosterone synthase gene (CYP11B2). The study aim was to analyze the association of Chronic Kidney Disease (CKD) with allelic polymorphism of the CYP11B2 at position -344 (-344C/T) in the promoter in patients with essential arterial hypertension (EAH). 72 subjects with EAH and target-organ damaging (2nd stage), moderate, high or very high cardiovascular risk were involved in the case-control study. Among them, 70.83% (51) females and 29.17% (21) males, mean age 59.87±8.02 yo; disease duration from 6 to 25 years. CKD was determined by the National Kidney Foundation recommendations (Kidney Disease: Improving Global Outcomes (KDIGO), 2012) after glomerular filtration rate (GFR) decline <60 ml/min/1,73 m2 for over 3 months (by Cockroft-Gault formula and CKD-EPI for Cystatin-C and Creatinine serum levels depending on gender). CKD was diagnosed in 29 persons. Control group consisted of fourty-eight practically healthy individuals of relevant age. Gene polymorphism of aldosterone synthase gene CYP11B2 (-344C/T) was examined by polymerase chain reaction (PCR). The probability of EAH in the observed population increased 1.49 times in T-allele carriers of CYP11B2 gene, but only in females [OR=1.90; 95%CI:1.02-3.54; р=0.029], with contrary decreasing in C-allele women (p=0.041). Moreover, T-allele increased probability of CKD (GFR<60 ml/min/1,73m2) in hypertensive population 1.48 times [OR=1.86; 95%CI:1.01-3.58; р=0.049], especially in T-allele females 1.53 times [OR=6.51; 95%CI:1.39-30.60; р=0.007] with low CKD risk in T-allele males [OR=0.15; 95%CI:0.03-0.72; р=0.009], respectively. Furthermore, some predictors like Diabetes, the 2nd and 3rd grades Obesity, and the 3rd grade of Blood Pressure elevation escalated the risk of CKD 2.4, 2.08-2.32 and 2.91 times, accordingly (p<0.05). Thus, aldosterone synthase gene CYP11B2 (-344C/T) associated with EAH. T-allele increased risk of CKD in hypertensive population, especially in females.

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Abstract P175: Chronic Exercise Attenuates Blood Pressure Elevation and Albuminuria With Improvement of Renal Lipid Metabolism in High Fructose-fed Rats

Hypertension ◽

10.1161/hyp.70.suppl_1.p175 ◽

2017 ◽

Vol 70 (suppl_1) ◽

Author(s):

Gaizun Hu ◽

Osamu Ito ◽

Lusi Xu

Keyword(s):

Blood Pressure ◽

Fatty Acid ◽

Lipid Metabolism ◽

Fatty Acid Synthase ◽

Control Group ◽

Chronic Exercise ◽

Blood Pressure Elevation ◽

Pressure Elevation ◽

High Fructose ◽

Renal Expression

High fructose diet (HFr) can lead to metabolic disorder, hypertension, and renal disease. Although chronic exercise (Ex) provides various beneficial effects on hypertension and kidney disease, the precise mechanism is not fully clarified. Thus, present study examined the effects of Ex on the blood pressure, renal function and renal lipid metabolism in rats fed with HFr. Sprague-Dawley rats were allocated to 3 groups. The HFr and Ex groups were fed with HFr (60%, w/w), the control group was fed with the diet in which fructose was replaced by starch. The Ex group underwent treadmill exercise at aerobic intensity. After 12 weeks, renal triglyceride (TG) content were measured, and expression of enzymes and regulators of fatty acid metabolism were analyzed by Western blot. HFr increased systolic blood pressure (SBP) and albuminuria and Ex decreased the HFr-increased SBP and albuminuria (85±4 vs. 122±9 vs. 91±4 mmHg, P<0.01, 326±67 vs. 534±79 vs. 176±54 mg/day, P<0.01). HFr increased plasma TG and uric acid (UA) and Ex decreased the HFr-increased TG and UA (124±20 vs. 474±35 vs. 238±23 mg/dL, P<0.01, 1.15±0.10 vs. 2.14±0.10 vs. 1.50±0.13 mg/dL, P<0.01), whereas HFr or Ex did not affect plasma creatinine. HFr increased renal TG content and Ex decreased the HFr-increased TG content (12.2±0.5 vs. 14.1±0.5 vs. 10.3±1.1 mg/100mg tissue, P<0.01). Among enzymes of fatty acid synthesis, HFr increased the renal expression of fatty acid synthase (FAS), and Ex decrease the expression of FAS (P<0.01). Among enzymes and regulators of fatty acid oxidation, HFr decreased the renal expression of PPARα, carnitine palmitoyltransferase I (CPTI), medium-chain acyl-CoA dehydrogenase (MCAD) (P<0.05), and Ex increased the expression of PPARα, CPTI, MCAD, and acyl-coenzyme A oxidase (ACOX). These results indicated that Ex attenuates blood pressure elevation, albuminuria with an improvement of renal lipid metabolism in the HFr-fed rats. These effects of Ex may relate to an improvement of the renal lipid metabolism.

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THE PERMEABILITY OF GLOMERULAR CAPILLARIES TO GRADED DEXTRANS

The Journal of Cell Biology ◽

10.1083/jcb.63.3.883 ◽

1974 ◽

Vol 63 (3) ◽

pp. 883-903 ◽

Cited By ~ 182

Author(s):

John P. Caulfield ◽

Marilyn G. Farquhar

Keyword(s):

Basement Membrane ◽

Mesangial Cells ◽

Left Kidney ◽

Permeability Barrier ◽

Structural Elements ◽

High Concentration ◽

Glomerular Permeability ◽

Sharp Drop ◽

High Concentrations ◽

Glomerular Capillaries

Graded dextrans have been used as tracers to identify the primary permeability barrier(s) to macromolecules among the structural elements (endothelium, mesangium, basement membrane, epithelium) of the glomerular capillary wall. Three narrow-range fractions of specified molecular weights and Einstein-Stokes radii (ESR) were prepared by gel filtration: (a) 32,000 mol wt, ESR = 38 Å; (b) 62,000 mol wt, ESR = 55 Å; and (c) 125,000 mol wt, ESR = 78 Å. These fractions are known to be extensively filtered, filtered in only small amounts, and largely retained, respectively, by the glomerular capillaries. Tracer solutions were infused i.v. into Wistar-Furth rats, and the left kidney was fixed after 5 min to 4 h. The preparations behaved as predicted: initially, all three fractions appeared in the urinary spaces, with 32,000 > 62,000 » 125,000. The smallest fraction was totally cleared from the blood and urinary spaces by 2.5 h, whereas the intermediate and largest fractions were retained in the circulation at high concentrations up to 4 h. With all fractions, when particles occurred in high concentration in the capillary lumina, they were present in similarly high concentrations in the endothelial fenestrae and inner (subendothelial) portions of the basement membrane, but there was a sharp drop in their concentration at this level—i.e., between the inner, looser portions of the basement membrane and its outer, more compact portions. With the two largest fractions, accumulation of particles occurred against the basement membrane in the mesangial regions with time. No accumulation was seen with any of the fractions in the epithelial slits or against the slit membranes. Dextran was also seen in phagosomes in mesangial cells, and in absorption droplets in the glomerular and proximal tubule epithelium. It is concluded that the basement membrane is the main glomerular permeability barrier to dextrans, and (since their behavior is known to be similar) to proteins of comparable dimensions (40,000–200,000 mol wt). The findings are discussed in relation to previous work using electron-opaque tracers to localize the glomerular permeability barrier and in relation to models proposed for the functions of the various glomerular structural elements.

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Burnout of the Mind – Burnout of the Body?

Journal of Psychophysiology ◽

10.1027/0269-8803/a000182 ◽

2018 ◽

Vol 32 (1) ◽

pp. 30-42 ◽

Cited By ~ 2

Author(s):

Claudia Traunmüller ◽

Kerstin Gaisbachgrabner ◽

Helmut Karl Lackner ◽

Andreas R. Schwerdtfeger

Keyword(s):

Blood Pressure ◽

Allostatic Load ◽

Maslach Burnout Inventory ◽

The Body ◽

Lower Percentage ◽

Control Group ◽

Urinary Catecholamines ◽

Morning Cortisol ◽

The Mind ◽

Cortisol Increase

Abstract. In the present paper we investigate whether patients with a clinical diagnosis of burnout show physiological signs of burden across multiple physiological systems referred to as allostatic load (AL). Measures of the sympathetic-adrenergic-medullary (SAM) axis and the hypothalamic-pituitary-adrenal (HPA) axis were assessed. We examined patients who had been diagnosed with burnout by their physicians (n = 32) and were also identified as burnout patients based on their score in the Maslach Burnout Inventory-General Survey (MBI-GS) and compared them with a nonclinical control group (n = 19) with regard to indicators of allostatic load (i.e., ambulatory ECG, nocturnal urinary catecholamines, salivary morning cortisol secretion, blood pressure, and waist-to-hip ratio [WHR]). Contrary to expectations, a higher AL index suggesting elevated load in several of the parameters of the HPA and SAM axes was found in the control group but not in the burnout group. The control group showed higher norepinephrine values, higher blood pressure, higher WHR, higher sympathovagal balance, and lower percentage of cortisol increase within the first hour after awakening as compared to the patient group. Burnout was not associated with AL. Results seem to indicate a discrepancy between self-reported burnout symptoms and psychobiological load.

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