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    Wyświetlanie 1-5 z 5
    Tytuł:
    Addition of ETA receptor blockade increases renoprotection provided by renin–angiotensin system blockade in 5/6 nephrectomized Ren-2 transgenic rats
    Addition of ETA receptor blockade increases renoprotecion provided by renin-angiotensin system blockade in5/6 nephrectomized
    Autorzy:
    Kramer, Hubert J.
    Huskova, Zdenka
    Kujal, Peter
    Sadowski, Janusz
    Vaneckova, Ivana
    Walkowska, Agnieszka
    Certikova-Chabova, Vera
    Skaroupkova, Petra
    Kompanowska-Jezierska, Elżbieta
    Vernerova, Zdenka
    Tesal, Vladimir
    Cervenka, Ludek
    Współwytwórcy:
    Department of Nephrology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic
    artment of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Poland of Institute of Physiology , Academy of Sciences of the Czech Republic, Prague
    Department of Pathology, 3rd Faculty of Medicine, Charles University, Prague, Czech Republicc Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republicd Section of Nephrology, Medical Policlinic, Department of Medicine, University of Bonn, Bonn, Germanye Department of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Polandf Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague
    Wydawca:
    Elsevier
    Powiązania:
    Life Sciences
    Opis:
    MS: There is evidence that in addition to hypertension and hyperactivity of the renin-angiotensin system (RAS), enhanced intrarenal activity of endothelin (ET) system contributes to the pathophysiology and progression of chronic kidney disease (CKD). This prompted us to examine if this progression would be alleviated by addition of type A ET receptor (ETA) blockade to the standard blockade of RAS.MAIN METHODS: Ren-2 transgenic rats (TGR) after 5/6 renal ablation (5/6 NX) served as a model of CKD. For RAS inhibition a combination of angiotensin-converting enzyme inhibitor (trandolapril, 6 mg/L drinking water) and angiotensin II type 1 receptor blocker (losartan, 100 mg/L drinking water) was used. Alternatively, ETA receptor blocker (atrasentan, 5 mg·kg(-1)·day(-1) in drinking water) was added to the combined RAS blockade. The follow-up period was 44 weeks after 5/6 NX, and the rats' survival rate, systolic blood pressure (SBP), proteinuria and indices of renal glomerular damage were evaluated.KEY FINDINGS: The survival rate was at first improved, by either therapeutic regime, however, the efficiency of RAS blockade alone considerably decreased 36 weeks after 5/6 NX: final survival rate of 65% was significantly lower than 91% achieved with combined RAS and ETA receptor blockade. SBP was not affected by the addition of ETA blockade while proteinuria and renal glomerular damage were further reduced.
    AIMS: There is evidence that in addition to hypertension and hyperactivity of the renin-angiotensin system (RAS), enhanced intrarenal activity of endothelin (ET) system contributes to the pathophysiology and progression of chronic kidney disease (CKD). This prompted us to examine if this progression would be alleviated by addition of type A ET receptor (ETA) blockade to the standard blockade of RAS.MAIN METHODS: Ren-2 transgenic rats (TGR) after 5/6 renal ablation (5/6 NX) served as a model of CKD. For RAS inhibition a combination of angiotensin-converting enzyme inhibitor (trandolapril, 6 mg/L drinking water) and angiotensin II type 1 receptor blocker (losartan, 100 mg/L drinking water) was used. Alternatively, ETA receptor blocker (atrasentan, 5 mg·kg(-1)·day(-1) in drinking water) was added to the combined RAS blockade. The follow-up period was 44 weeks after 5/6 NX, and the rats' survival rate, systolic blood pressure (SBP), proteinuria and indices of renal glomerular damage were evaluated.KEY FINDINGS: The survival rate was at first improved, by either therapeutic regime, however, the efficiency of RAS blockade alone considerably decreased 36 weeks after 5/6 NX: final survival rate of 65% was significantly lower than 91% achieved with combined RAS and ETA receptor blockade. SBP was not affected by the addition of ETA blockade while proteinuria and renal glomerular damage were further reduced.SIGNIFICANCE: Our data show that a combined RAS and ETA receptor blockade exhibits additional beneficial effects on survival rate and the progression of CKD in 5/6 NX TGR, as compared with RAS inhibition alone.
    Dostawca treści:
    RCIN - Repozytorium Cyfrowe Instytutów Naukowych
    Książka
    Tytuł:
    Neuroendocrine activation as a target of modern chronic heart failure pharmacotherapy
    Autorzy:
    Thor, Piotr
    Dobrek, Łukasz
    Opis:
    At present, a constant progress in pathophysiology understanding and treatment of the chronic heart failure (CHF) is arising. The current CHF pharmacotherapy is complex, involving factors affecting the reninangiotensin- aldosterone system (RAAS), β-blockers, diuretics and vasodilatators. There are also significant efforts to introduce in CHF pharmacology novel therapeutic strategies, based on the other neurohormonal mechanisms activated in CHF. They include vasopressin receptor antagonists (VRA; vaptans), endothelin receptor antagonists (ERA; sentans), agents relating to the natriuretic peptides system (neutral endopeptidase inhibitors; NEPI and vasopeptidase inhibitors; VPI) and anticytokines agents (anti TNF-α immunoglobulin or TNF-α scavenger receptor; Etanercept). In this article we briefly describe the modern approach to CHF systemic treatment.
    Dostawca treści:
    Repozytorium Uniwersytetu Jagiellońskiego
    Artykuł
    Autorzy:
    Kij, Agnieszka
    Walczak, Maria
    Kuś, Kamil
    Chłopicki, Stefan
    Zakrzewska, Agnieszka
    Suraj, Joanna
    Opis:
    Endothelial dysfunction has prognostic, diagnostic and therapeutic significance in cardiovascular disease, but the endothelial phenotype is still not measured routinely to stratify the cardiovascular risk and tailor therapy. Flow-mediated dilation (FMD), the gold-standard technique for the functional assessment of endothelial function that is increasingly used in clinical settings measures the nitric oxide (NO)-dependent function only. However, the endothelial dysfunction involves a plethora of pathophysiologically important biochemical changes beyond alterations in the NO bioavailability. Still, in many diseases, some plasma protein biomarkers reflecting the pro-thrombotic and the pro-inflammatory endothelial phenotypes have poor selectivity, specificity, and a weak predictive value if they are used alone. Therefore, a multi biomarker strategy seems to be a reasonable and promising alternative. Here, we propose a multi-biomarker strategy to diagnose the endothelial dysfunction and to monitor the efficacy of an endothelium-targeted therapy. This strategy is based on the panel of endothelial biomarkers, reflecting various aspects and mechanisms of dysfunctional endothelium. The potential of an advanced analytical platform like the ultra-high performance liquid chromatography (UHPLC) coupled to mass spectrometry-based multiple reaction monitoring for simultaneous quantification of multiple endothelial biomakers is also discussed.
    Dostawca treści:
    Repozytorium Uniwersytetu Jagiellońskiego
    Artykuł
      Wyświetlanie 1-5 z 5

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