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Journal Article 2005; 26(3): 242-246 PubMed PMID: 15990729 Citation  Keywords:  Adolescent, Biomarkers:blood, C-Reactive Protein:metabolism, Child, Endothelium, Vascular:immunology, Female, Humans, Hypertension:etiology, Intercellular Adhesion Molecule-1:blood, Interleukin-1:blood, Interleukin-6:blood, Lipids:blood, Male, Obesity:com.   

OBJECTIVES: It has been suggested that a rise in blood pressure (BP) causes low-grade inflammation of the endothelium which, in turn, may be responsible for further damage of endothelium and worsening of BP control. The aim of the study was to evaluate serum levels of inflammation and endothelial activation markers in children with obesity-related hypertension and normotensive controls in relation to other traditional risk factors of arterial hypertension.

METHODS: Plasma insulin, glucose, C-reactive protein (CRP), fibrinogen (FB) interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and lipids levels were determined in 50 children with obesity-related hypertension and 143 obese children with normal BP. Insulin resistance was assessed by the homeostasis model.

RESULTS: Children with hypertension had significantly higher levels of all inflammatory markers as well as endothelial activation indices compared with normotensive subjects. In the stepwise regression model significant independent correlates for systolic BP were CRP, FB, VCAM-1, HOMA IR, LDL cholesterol and fat mass, whereas CRP, IL-6, ICAM-1, FB, LDL and HDL cholesterol were the determinants of diastolic BP in children with obesity-related hypertension.

CONCLUSION: These results indicate that low-grade inflammation and endothelial dysfunction are closely involved in the pathogenesis of obesity-related hypertension relatively early in life....

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Journal Article 2003; 24(6): 479-498 PubMed PMID: 15073580 Citation  Keywords:  Humans, Hypertension:diagnosis, Neuroendocrinology:trends, Periodicity,.   

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Journal Article 2003; 24(6): 431-434 PubMed PMID: 15073570 Citation  Keywords:  Adult, Anorexia Nervosa:metabolism, Appetite:physiology, Diabetes Mellitus:metabolism, Feedback, Physiological, Female, Glucose Tolerance Test, Human Growth Hormone:metabolism, Humans, Hypertension:metabolism, Leptin:blood, Luteinizing Hormone:metabolism,.   

OBJECTIVE: It has been reported that neuropeptides may play a role in the control of appetite and in the mechanism of hormone release. Neuropeptides such as beta-endorphin, neuropeptide Y (NPY), galanin and leptin may affect hormones release, on the other hand the hormonal status may modulate neuropeptide activity.

METHODS: The material consisted of 90 obese women, 30 women with Anorexia Nervosa, and 30 healthy, lean women of control group. Plasma beta-endorphin, NPY, leptin, somatostatin and serum pituitary and gonadal hormones concentrations were measured with RIA methods.

RESULTS: We observed the highest plasma NPY levels in obese hypertensive and diabetic patients. After carbohydrate administration (OGTT) a marked increase of insulin, beta-endorphin and NPY was found. The blunted response of GH to GH-RH may be connected with increased somatostatin activity and hyperinsulinemia. The abnormal response of LH to opioid blockade may be a result of disturbed opioid and NPY activities in obese patients. However in patients with anorexia nervosa, plasma leptin and NPY concentrations were low. The disturbances in beta-endorphin release are also observed.

CONCLUSIONS: The neuroendocrine disturbances in obesity and in anorexia nervosa are opposite. The feedback mechanism between leptin and NPY is disturbed in both in obesity and in anorexia nervosa. An abnormal activity of neuropeptides may lead to disturbed control of appetite and hormonal dysregulation in eating disorders....

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Journal Article 2003; 24(5): 339-340 PubMed PMID: 14647008 Citation  Keywords:  Blood Pressure, Blood Pressure Monitoring, Ambulatory:standards, Circadian Rhythm, Heart Rate, Humans, Hypertension:diagnosis, Seasons,.   

: The diagnoses of summer or winter hypertension in one and the same person can depend upon the clock hour of measurement....

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Journal Article 2003; 24(5): 325-328 PubMed PMID: 14647005 Citation  Keywords:  Aldosterone:urine, Blood Pressure:genetics, Genetic Markers, Humans, Hypertension, Renal:genetics, Insulin:genetics, Middle Aged, Minisatellite Repeats, Phenotype, Pilot Projects, Polymorphism, Restriction Fragment Length, Potassium:urine, Quantitative Tr.   

BACKGROUND: Blood pressure regulation is a complex process influenced by numerous environmental and genetic factors. Consequently, there's no cookie-cutter approach for the elucidation of of the genetic mechanism involved. One of the goals of molecular geneticists in the field of hypertension is to unravel the genetic architecture of blood pressure regulation.

METHODS: With the aim of identifying quantitative trait loci participating in the control of blood pressure, we carried out a pilot study on a sample population of middle-aged, U.S. Caucasians (44 subjects). The design of the study was to search for associations between clinical variables of blood pressure regulation pertaining to the renin-angiotensin-aldosterone system (systolic and diastolic blood pressures, urinary excretion of sodium, potassium and aldosterone, plasma renin activity) and a genetic marker at a candidate gene locus - the human insulin gene (INS) RESULTS: We observed significant associations between a variable number of tandem repeats (VNTR) marker (visualized as a biallelic, class I/class III marker system) localized at the 5' end of the human INS gene, and plasma renin activity and urinary sodium, potassium and aldosterone.

CONCLUSION: Our results indicate that between 6 and 10 QTLs with comparable effects could be involved in blood pressure regulation via the rennin angiotensin system....

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Journal Article 2018; 39(3): 209-218 PubMed PMID: 30431738 Citation  Keywords:  Animals, Behavior, Animal, Blood-Brain Barrier:metabolism, Brain:diagnostic imaging, Brain Edema:etiology, Disease Models, Animal, Evans Blue, Intracranial Hypertension:etiology, Locomotion, Male, Myelin Sheath:pathology, Permeability, Rats, Rats, Wistar,.   

OBJECTIVES: This paper presents our own rat model of the cellular brain edema, induced by water intoxication (WI). The basic principle of the model is an osmotic imbalance in the cell membrane followed by an intracellular flow of sodium and simultaneous accumulation of water leading to the subsequent increase of BBB permeability. METHODS: The usefulness of the model was tested in precisely specified conditions whose results were clearly expressed. The procedure determined both how WI induces cellular edema as well as the disturbances caused by cellular edema. RESULTS: The evidence of existing cellular edema with increased BBB permeability was proved by intracellular accumulation of intravital dye with a large molecular size; increased brain-water content was confirmed by using the dry/wet weight method and by the decrease in CT density; the elevated intracranial pressure (ICP) due to the expanding volume was determined by continuous monitoring the ICP; the structural lesions were proved by identification of the myelin disintegration; and the impaired nervous functions was demonstrated by the of open field test method. CONCLUSION: Our experimental model can help the future studies of pathophysiology of cellular brain edema and is suitable for testing neuroprotective agents....

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