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  • 1
    Language: English
    In: American journal of hypertension, 2001-04, Vol.14 (S1), p.227A-227A
    Description: ETA receptors have been implicated in obesity-associated hypertension (Hypertension 1999; 33: 1169). We characterized the renal endothelin system in diet-induced obesity and determined the effects of chronic treatment with the ETA antagonist darusentan. C57BL/6J mice were fed a standard diet (control) or a high-fat diet (Harlan TD88137) with or without darusentan (50 mg/kg/d, 30 wk). Total RNA was extracted from whole kidneys and mRNA expression of preproendothelin-1 (ppET-1), ETA receptors, and β-actin were determined by RT-PCR using mouse-specific primers. PCR-products were normalized vs. β-actin or 18S rRNA. Renal ET-1 protein was measured by RIA/HPLC. High fat diet increased body weight by 257% compared to 54% (control diet). Darusentan had no effect on body weight in obese mice (263%) and treatments had no effect on systolic blood pressure. Obesity was associated with upregulation of renal ETA receptors (144±5% vs 100±7%, p〈0.05 vs. control) and to a lesser extent, preproendothelin-1 (113±5% vs.100±2%, p〈0.05 vs. control). In obese mice chronic darusentan treatment in part prevented the ETA receptor upregulation (126% vs. 144±5%, p〈0.05) but had no significant effect on ppET-1 mRNA expression (101±9 vs. 100±2%, n.s.). Renal ET-1 protein increased in obese animals (from 190±18 to 267±19 pg/g tissue, p〈0.05 vs. control). This increase was not affected by concomitant darusentan treatment (n.s.). These data for the first time demonstrate that obesity in normotensive rats is associated with upregulation of renal ETA receptor expression suggesting that body weight per se affects ET receptor expression in the kidney. Our data further indicate that in this model ETA receptors control expression of the ETA receptor but not the ppET-1 gene, suggesting autocrine regulation in vivo. These mechanisms might contribute to the pathogenesis of obesity-associated diseases affecting the kidney and/or blood pressure.
    Subject(s): hypertension ; kidney ; obesity
    ISSN: 0895-7061
    E-ISSN: 1879-1905
    Source: Alma/SFX Local Collection
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  • 2
    Language: English
    In: Hypertension (Dallas, Tex. 1979), 1999-04, Vol.33 (4), p.954-960
    Description: Abstract —In isolated cardiac myocytes, the direct effects of angiotensin II on cellular growth and gene expression were shown to be mediated by endothelin via the endothelin subtype A (ET A ) receptor. To determine whether this pathway is also involved in the cardiovascular adaptations to a chronic activation of the renin-angiotensin system in vivo, the effects of a selective ET A receptor antagonist (LU 127043) were investigated in adult rats with renal artery stenosis. Four groups of rats (n=107) were studied over a period of 10 days after surgery: (1) sham-operated animals with saline administration, (2) rats subjected to left renal artery clipping with saline administration, (3) sham-operated rats with LU 127043 administration, and (4) rats subjected to left renal artery clipping with LU 127043 administration. LU 127043 (50 mg/kg) or saline was given by gavage twice daily starting 1 day before the operation. In clipped rats with saline administration, plasma renin activity, the ratio of left ventricular weight to body weight, and mRNAs for β-myosin heavy chain and atrial natriuretic peptide were significantly elevated as early as 2 days after surgery. Blood pressure started to rise on the third postoperative day and attained a steady state hypertensive level by day 6. Blockade of ET A receptors had no effects on plasma renin activity or the time course of hypertension in clipped animals but completely prevented left ventricular hypertrophy and the re-expression of the β-myosin heavy chain and atrial natriuretic peptide genes on day 2. While the expressions of the β-myosin heavy chain and atrial natriuretic peptide genes were not different from saline-treated, clipped animals after day 4, the development of left ventricular hypertrophy remained markedly blunted (−50%) during ET A receptor blockade until day 10. These results show that a continuous blockade of ET A receptors significantly attenuates the development of left ventricular hypertrophy and, more transiently, fetal gene expression in the early phase of renovascular hypertension. Since neither blood pressure nor the increase in plasma renin activity was significantly altered by ET A receptor blockade, the inhibitory influences of the ET A receptor antagonist on left ventricular hypertrophy and gene expression were mediated most likely through a direct blockade of myocardial ET A receptors.
    ISSN: 0194-911X
    E-ISSN: 1524-4563
    Source: Hellenic Academic Libraries Link
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
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  • 3
    Language: English
    In: Hypertension (Dallas, Tex. 1979), 2004-12, Vol.44 (6), p.974-981
    Description: The cause of focal-segmental glomerulosclerosis as a consequence of physiological aging, which is believed to be inexorable, is unknown. This study investigated whether inhibition of endothelin-1, a growth-promoting peptide contributing to renal injury in hypertension and diabetes, affects established glomerulosclerosis and proteinuria in the aged kidney. We also determined the role of endothelin receptors for podocyte injury in vivo and in vitro. Aged Wistar rats, a model of spontaneous age-dependent glomerulosclerosis, were treated with the orally active endothelin subtype A (ETA) receptor antagonist darusentan, and evaluation of renal histology, renal function studies, and expression analyses were performed. In vitro experiments using puromycin aminonucleoside to induce podocyte injury investigated the role of ETA receptor signaling for apoptosis, cytoskeletal injury, and DNA synthesis. In aged Wistar rats, established glomerulosclerosis and proteinuria were reduced by 〉50% after 4 weeks of darusentan treatment, whereas blood pressure, glomerular filtration rate, or tubulo-interstitial renal injury remained unaffected. Improvement of structural injury in glomeruli and podocytes was accompanied by a reduction of the expression of matrix metalloproteinase-9 and p21. In vitro experiments blocking ETA receptors using specific antagonists or RNA interference prevented apoptosis and structural damage to podocytes induced by puromycin aminonucleoside. In conclusion, these results support the hypothesis that endogenous endothelin contributes to glomerulosclerosis and proteinuria in the aging kidney. The results further suggest that age-dependent glomerulosclerosis is not merely a “degenerative” but a reversible process locally confined to the glomerulus involving recovery of podocytes from previous injury.
    Subject(s): Aging - physiology ; Animals ; Antihypertensive agents ; Apoptosis ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Cardiovascular system ; Cell Cycle Proteins - genetics ; Cyclin-Dependent Kinase Inhibitor p21 ; Disease Models, Animal ; DNA - biosynthesis ; Endothelin A Receptor Antagonists ; Endothelin-1 - antagonists & inhibitors ; Endothelin-1 - physiology ; Experimental diseases ; Gene Expression ; Gene Silencing ; Glomerular Filtration Rate ; Glomerulosclerosis, Focal Segmental - drug therapy ; Glomerulosclerosis, Focal Segmental - pathology ; Glomerulosclerosis, Focal Segmental - physiopathology ; Kidney - cytology ; Kidney - drug effects ; Kidney - physiology ; Kidney Glomerulus - metabolism ; Kidney Glomerulus - pathology ; Male ; Matrix Metalloproteinase 9 - genetics ; Medical sciences ; Pharmacology. Drug treatments ; Phenylpropionates - pharmacology ; Proteinuria - drug therapy ; Proteinuria - etiology ; Pyrimidines - pharmacology ; Rats ; Rats, Wistar ; Receptor, Endothelin A - physiology ; Signal Transduction
    ISSN: 0194-911X
    E-ISSN: 1524-4563
    Source: Hellenic Academic Libraries Link
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
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  • 4
    Language: English
    In: Laboratory investigation, 2003-09, Vol.83 (9), p.1267-1277
    Description: The pathomechanisms that cause renal damage in diabetes have not been completely clarified. Treatment with angiotensin-converting enzyme inhibitors (ACE-i) is highly effective but fails to completely prevent end-stage renal disease. The effects of ET(A)-receptor blockers (ET(A)-RB) on renal damage are controversial and have rarely been investigated in type 2 diabetes. We compared the influence of the selective ET(A)-RB LU135252 and the ACE-i Trandolapril on renal structure in the SHR/N-cp rat model of type 2 diabetes. Three-month-old male SHR/N-cp rats were left untreated or received daily either Trandolapril or LU135252. The experiment was terminated after 6 months. The glomerulosclerosis index; tubulointerstitial damage index; and glomerular geometry, glomerular cell number, and capillary density were investigated. Proliferating cell nuclear antigen and desmin expression of podocytes, renal mRNA expression of endothelin (ET-1) and transforming growth factor-beta, blood pressure, and urine albumin excretion were measured. The glomerulosclerosis index was significantly higher in untreated diabetic animals than in the groups that were treated with ACE-i and ET(A)-RB. There were analogous changes in tubulointerstitial damage index. Treatment with either substance comparably lowered urinary albumin excretion in diabetic SHR/N-cp. Podocyte and endothelial cell numbers per glomerulus decreased in untreated diabetic animals; this was prevented by the ACE-i but not by the ET(A)-RB. Glomerular capillary length density was lower in SHR/N-cp, and this was normalized by ACE-i only. Increased expression of desmin and proliferating cell nuclear antigen expression of podocytes in the SHR/N-cp was abrogated by ACE-i but not by ET(A)-RB. Treatment with ACE-i or ET(A)-receptor antagonist resulted in less structural and functional alterations, but the ET(A)-RB was inferior to the ACE-i. This is particularly the case for podocyte changes pointing to angiotensin II-dependent pathomechanisms.
    Subject(s): Albuminuria ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Animals ; Associated diseases and complications ; Biological and medical sciences ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - pathology ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - pathology ; Diabetes. Impaired glucose tolerance ; Diabetic Nephropathies - drug therapy ; Diabetic Nephropathies - etiology ; Diabetic Nephropathies - pathology ; Disease Models, Animal ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endothelin Receptor Antagonists ; Endothelin-1 - genetics ; Endothelin-1 - metabolism ; Immunohistochemistry ; Indoles - therapeutic use ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Male ; Medical sciences ; Phenylpropionates - therapeutic use ; Proliferating Cell Nuclear Antigen - metabolism ; Pyrimidines - therapeutic use ; Rats ; RNA, Messenger - metabolism ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - metabolism
    ISSN: 0023-6837
    E-ISSN: 1530-0307
    Source: Alma/SFX Local Collection
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  • 5
    Language: English
    In: American Journal of Physiology - Heart and Circulatory Physiology, 1999-03-01, Vol.276 (3), p.1022-1027
    Description: The role of endothelin (ET)-1 in blood pressure homeostasis and the interaction with the renin-angiotensin system (RAS) was investigated in normotensive conscious dogs. ETAreceptors were blocked by LU-135252 (1–30 mg/kg); trandolapril (2 mg/kg) or losartan (10 mg/kg) was used to inhibit the RAS. LU-135252 in oral doses of 3–30 mg/kg significantly reduced mean arterial pressure (MAP) by ∼10 mmHg maximally, whereas trandolapril or losartan were without any effect. MAP reduction was more pronounced when LU-135252 was combined with either losartan (−15.5 ± 3.2 mmHg; 2 h postadministration;P 〈 0.05) or trandolapril (−30.9 ± 3.6 mmHg; P 〈 0.05). When endogenous nitric oxide (NO) generation was blocked but NO concomitantly infused, this synergistic effect on MAP was prevented. The data show that ET-1 contributes to the maintenance of blood pressure via ETA receptors. Furthermore, ET-1 and ANG II play a prominent role in the control of blood pressure by opposing the effects of NO. The pronounced blood pressure fall after combined blockade of ETA receptors and the RAS may be mediated by an enhanced release of NO.
    ISSN: 0363-6135
    E-ISSN: 1522-1539
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
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  • 6
    Language: English
    In: Proceedings of the National Academy of Sciences - PNAS, 1998-11-24, Vol.95 (24), p.14367-14372
    Description: This study investigated whether endothelin-1 (ET-1), a potent vasoconstrictor, which also stimulates cell proliferation, contributes to endothelial dysfunction and atherosclerosis. Apolipoprotein E (apoE)-deficient mice and C57BL/6 control mice were treated with a Western-type diet to accelerate atherosclerosis with or without ET A receptor antagonist LU135252 (50 mg/kg/d) for 30 wk. Systolic blood pressure, plasma lipid profile, and plasma nitrate levels were determined. In the aorta, NO-mediated endothelium-dependent relaxation, atheroma formation, ET receptor-binding capacity, and vascular ET-1 protein content were assessed. In apoE-deficient but not C57BL/6 mice, severe atherosclerosis developed within 30 wk. Aortic ET-1 protein content ( P 〈 0.0001) and binding capacity for ET A receptors was increased as compared with C57BL/6 mice. In contrast, NO-mediated, endothelium-dependent relaxation to acetylcholine (56 ± 3 vs. 99 ± 2%, P 〈 0.0001) and plasma nitrate were reduced (57.9 ± 4 vs. 93 ± 10 μmol/liter, P 〈 0.01). Treatment with the ET A receptor antagonist LU135252 for 30 wk had no effect on the lipid profile or systolic blood pressure in apoE-deficient mice, but increased NO-mediated endothelium-dependent relaxation (from 56 ± 3 to 93 ± 2%, P 〈 0.0001 vs. untreated) as well as circulating nitrate levels (from 57.9 ± 4 to 80 ± 8.3 μmol/liter, P 〈 0.05). Chronic ET A receptor blockade reduced elevated tissue ET-1 levels comparable with those found in C57BL/6 mice and inhibited atherosclerosis in the aorta by 31% without affecting plaque morphology or ET receptor-binding capacity. Thus, chronic ET A receptor blockade normalizes NO-mediated endothelial dysfunction and reduces atheroma formation independent of plasma cholesterol and blood pressure in a mouse model of human atherosclerosis. ET A receptor blockade may have therapeutic potential in patients with atherosclerosis.
    Subject(s): Acetylcholine - pharmacology ; Animals ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - pathology ; Aorta, Thoracic - physiopathology ; Apolipoproteins E - deficiency ; Arteriosclerosis - pathology ; Arteriosclerosis - physiopathology ; Arteriosclerosis - prevention & control ; Biological Sciences ; Blood Pressure - drug effects ; Cardiovascular disease ; Cholesterol - blood ; Diet ; Endothelin Receptor Antagonists ; Endothelin-1 - blood ; Endothelin-1 - pharmacology ; Endothelin-1 - physiology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Endothelium, Vascular - physiopathology ; Humans ; In Vitro Techniques ; Lipoproteins - blood ; Male ; Medical research ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - pathology ; Muscle, Smooth, Vascular - physiopathology ; Nitric Oxide - physiology ; Nitroprusside - pharmacology ; Norepinephrine - pharmacology ; Phenylpropionates - pharmacology ; Pyrimidines - pharmacology ; Receptor, Endothelin A ; Rodents ; Species Specificity ; Systole ; Triglycerides - blood ; Vasodilation - drug effects
    ISSN: 0027-8424
    E-ISSN: 1091-6490
    Source: JSTOR Life Sciences
    Source: HighWire Press (Free Journals)
    Source: Hellenic Academic Libraries Link
    Source: PubMed Central
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  • 7
    Language: English
    In: British journal of pharmacology, 1997, Vol.120 (7), p.1335-1343
    Description: 1. Systemic infusion of neuropeptide Y (NPY) reduces renal blood flow and can concomitantly increase diuresis, natriuresis and calciuresis in anaesthetized rats. The present study was designed to investigate whether the apparently contradictory NPY effects on renal blood flow and urine formation and composition are mediated by distinct NPY receptor subtypes. 2. NPY and its analogues, peptide YY (PYY), [Leu31, Pro34]NPY and NPY13-36, were infused in incremental doses of 0.3, 1 and 3 micrograms kg-1 min-1 for 45 min each and the results compared to those obtained in vehicle-infused rats. Renal blood flow was monitored in 1-5 min intervals, while urine excretion and composition were determined in 15 min collection periods. Plasma renin activity and aldosterone concentrations were measured at the end of the final infusion period. 3. Relative to vehicle NPY, PYY and [Leu31, Pro34]NPY dose-dependently reduced renal blood flow and increased diuresis, natriuresis and calciuresis with roughly similar potency; NPY13-36 slightly but significantly increased renal blood flow but had no effect on diuresis, natriuresis and calciuresis. None of the peptides significantly affected endogenous creatinine clearance or kaliuresis. 4. Plasma renin activity was significantly reduced by PYY. Quantitatively similar reductions were observed with NPY and [Leu31, Pro34]NPY but failed to reach statistical significance with the given number of experiments. NPY13-36 did not reduce plasma renin activity. None of the peptides significantly affected plasma aldosterone concentrations. 5. In another series of experiments infusion of PYY3-36 (2 micrograms kg-1 min-1 for 120 min) did not reduce renal blood flow but significantly enhanced diuresis and natriuresis to a similar extent as the NPY 2 micrograms kg-1 min-1. 6. In a final series of experiments the Y1-selective antagonist, BIBP 3226 (1 or 10 micrograms kg-1 min-1) dose-dependently antagonized reductions of renal blood flow elicited by bolus injections of NPY (0.1-30 micrograms kg-1). BIBP 3226 (10 micrograms kg-1 min-1) also inhibited the effects of a 120 min infusion of NPY (2 micrograms kg-1 min-1) on renal blood flow but had only minor inhibitory effects on enhancements of diuresis and did not significantly affect enhancements of natriuresis. 7. We conclude that NPY reduces renal blood via a classical Y1 subtype of NPY receptor. In contrast enhancements of diuresis, natriuresis and calciuresis occur via a distinct subtype which resembles the receptor that mediates NPY-induced enhancement of food intake
    Subject(s): Animals ; Arginine - analogs & derivatives ; Arginine - pharmacology ; BIBP 3226 ; Biological and medical sciences ; diuresis ; Fundamental and applied biological sciences. Psychology ; Kidney - blood supply ; Kidney - drug effects ; Male ; natriuresis ; Neuropeptide Y ; Neuropeptide Y - pharmacology ; Papers ; Peptide Fragments ; Peptide YY ; Peptides - pharmacology ; Rats ; Rats, Wistar ; receptor subtypes ; Receptors, Neuropeptide Y - classification ; Receptors, Neuropeptide Y - drug effects ; Receptors, Neuropeptide Y - physiology ; Regional Blood Flow - drug effects ; renal blood flow ; Vertebrates: urinary system
    ISSN: 0007-1188
    E-ISSN: 1476-5381
    Source: Wiley Online Library All Journals
    Source: PubMed Central
    Source: Alma/SFX Local Collection
    Source: Get It Now
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  • 8
    Language: English
    In: Kidney international, 1999-02, Vol.55 (2), p.512-519
    Description: Endothelin receptor antagonists influence cardiovascular morphology in uremic rats. It is generally held that renal failure results in blood pressure (BP)-independent structural changes of the myocardium and the vasculature. The contribution, if any, of endothelin (ET) to these changes has been unknown. We morphometrically studied random samples of the left ventricle myocardium and small intramyocardial arteries in subtotally (5/6) nephrectomized (SNx) male Sprague-Dawley rats treated with either the selective ETA receptor antagonist BMS182874 (30mg/kg/day) or the nonselective ETA/ETB receptor antagonist Ro46-2005 (30mg/kg/day) in comparison with either sham-operated rats, untreated SNx, or SNx rats treated with the angiotensin-converting enzyme inhibitor trandolapril (0.1mg/kg/day). Eight weeks later, systolic BP was lower in trandolapril-treated SNx compared with untreated SNx animals. No decrease in BP was seen following either ET receptor antagonist at the dose used. A significantly increased volume density of the myocardial interstitium was found in untreated SNx rats as compared with sham-operated controls. Such interstitial expansion was prevented by trandolapril and either ET receptor antagonist. SNx caused a substantial increase in the wall thickness of small intramyocardial arteries. The increase was prevented by trandolapril or BMS182874 treatment. The arteriolar wall:lumen ratio was significantly lower in all treated groups when compared with untreated SNx. In contrast, only trandolapril, but not the ET receptor antagonists, attenuated thickening of the aortic media in SNx animals. The ETA-selective and ETA/ETB-nonselective receptor antagonists appear to prevent development of myocardial fibrosis and structural changes of small intramyocardial arteries in experimental chronic renal failure. This effect is independent of systemic BP.
    Subject(s): Animals ; Arteries - drug effects ; Arteries - pathology ; Biological and medical sciences ; blood pressure ; Coronary Vessels - drug effects ; Coronary Vessels - pathology ; Dansyl Compounds - pharmacology ; Endothelin Receptor Antagonists ; fibrosis ; Fundamental and applied biological sciences. Psychology ; Heart ; Heart - drug effects ; hypertension ; Male ; Medical sciences ; myocardial arteries ; Myocardium - pathology ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Pyrimidines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Renal failure ; subtotal nephrectomy ; Sulfonamides - pharmacology ; uremia ; Uremia - pathology ; Vertebrates: cardiovascular system
    ISSN: 0085-2538
    E-ISSN: 1523-1755
    Source: Alma/SFX Local Collection
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  • 9
    Language: English
    In: Hypertension (Dallas, Tex. 1979), 2000-01, Vol.35 (1, Part 2 Suppl), p.329-329
    Description: ABSTRACTIn the C57BL/6J mice model, we investigated whether obesity affects the function or expression of components of the tissue renin-angiotensin system and whether endothelin (ET)-1 contributes to these changes. ACE activity (nmol · L His-Leu · mg protein) was measured in lung, kidney, and liver in control (receiving standard chow) and obese animals treated for 30 weeks with a high-fat, low cholesterol diet alone or in combination with LU135252, an orally active ETA receptor antagonist. ACE mRNA expression was measured in the kidney, and the effects of LU135252 on purified human ACE were determined. Aortic and renal tissue ET-1 protein content was measured, and the vascular contractility to angiotensin II was assessed. Obesity was associated with a tissue-specific increase in ACE activity in the kidney (55±4 versus 33±3 nmol/L) but not in the lung (34±2 versus 32±2 nmol/L). Long-term LU135252 treatment completely prevented this activation (13.3±0.3 versus 55±4 nmol/L, P 〈0.05) independent of ACE mRNA expression, body weight, or renal ET-1 protein but did not affect pulmonary or hepatic ACE activity. Obesity potentiated contractions in response to angiotensin II in the aorta (from 6±2% to 33±5% KCl) but not in the carotid artery (4±1% to 3.6±1% KCl), an effect that was completely prevented with LU135252 treatment (6±0.4% versus 33±5% KCl). No effect of LU135252 on purified ACE was observed. Thus, obesity is associated with the activation of renal ACE in vivo independent of its mRNA expression and enhanced vascular contractility to angiotensin II. These effects are regulated by ET in an organ-specific manner, providing novel mechanisms by which ET antagonists may exert organ protection.
    Subject(s): Angiotensin II - pharmacology ; Animals ; Aorta - chemistry ; Aorta - cytology ; Aorta - enzymology ; Blood Pressure - drug effects ; Carotid Arteries - chemistry ; Carotid Arteries - cytology ; Carotid Arteries - enzymology ; Cholesterol - blood ; Cyclooxygenase Inhibitors - pharmacology ; Diet ; Endothelin Receptor Antagonists ; Endothelin-1 - analysis ; Endothelin-1 - metabolism ; Gene Expression Regulation, Enzymologic ; Humans ; Indomethacin - pharmacology ; Kidney - enzymology ; Lung - enzymology ; Male ; Mice ; Mice, Inbred C57BL ; Obesity - enzymology ; Organ Culture Techniques ; Peptidyl-Dipeptidase A - genetics ; Peptidyl-Dipeptidase A - metabolism ; Phenylpropionates - pharmacology ; Protein Binding - physiology ; Pyrimidines - pharmacology ; Receptor, Endothelin A ; Renin-Angiotensin System - physiology ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Thromboxane A2 - analogs & derivatives ; Thromboxane A2 - pharmacology ; Vasoconstriction - drug effects ; Vasoconstriction - physiology ; Vasoconstrictor Agents - pharmacology
    ISSN: 0194-911X
    E-ISSN: 1524-4563
    Source: Hellenic Academic Libraries Link
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
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  • 10
    Language: English
    In: Bioelectromagnetics, 2011-05, Vol.32 (4), p.291-301
    Description: The production of spindle disturbances in a human–hamster hybrid (AL) cell line by an electromagnetic field (EMF) with field strength of 90 V/m at a frequency of 900 MHz was studied in greater detail. The experimental setup presented allows investigating whether either the electrical (E) and/or the magnetic (H) field component of EMF can be associated with the effectiveness of the spindle‐disturbing potential. Therefore, both field components of a transversal electromagnetic field (TEM) wave have been separated during exposure of the biological system. This procedure should give more insight on understanding the underlying mechanisms of non‐thermal effects of EMF. A statistical comparison of the proportions of the fractions of ana‐ and telophases with spindle disturbances, obtained for five different exposure conditions with respect to unexposed controls (sham condition), showed that only cells exposed to the H‐field component of the EMF were not different from the control. Therefore, the results of the present study indicate that an exposure of cells to EMF at E‐field strengths of 45 and 90 V/m, as well as to the separated E component of the EMF, induces significant spindle disturbances in ana‐ and telophases of the cell cycle. Bioelectromagnetics 32:291–301, 2011. © 2010 Wiley‐Liss, Inc.
    Subject(s): Anaphase - radiation effects ; Animals ; Cell Line ; Cell Phone ; Cricetinae ; dosimetry ; electrical component ; Electricity - adverse effects ; EMF ; Humans ; Hybrid Cells - cytology ; Hybrid Cells - pathology ; Hybrid Cells - radiation effects ; Magnetics ; Radio Waves - adverse effects ; spindle disturbances ; Telophase - radiation effects
    ISSN: 0197-8462
    E-ISSN: 1521-186X
    Source: Hellenic Academic Libraries Link
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