National Repository of Grey Literature 5 records found  Search took 0.01 seconds. 
COVID-19 and kidney diseases
Stanovský, Samuel ; Čertíková-Chábová, Věra (advisor) ; Zahrádka, Ivan (referee)
In clinical practice, SARS-CoV-2 virus infection and COVID-19 disease are mainly associated with dominant respiratory disorders of varying severity, from minor events such as upper respiratory tract infections to life-threatening respiratory failure. However, COVID-19 can not only be seen as a respiratory infection, but the possibility of systemic involvement should also be considered. One of the internal organs that can be directly affected by the virus is the kidneys. Renal damage from the SARS-CoV-2 virus can occur in completely intact kidneys or can affect kidneys with pre-existing nephropathy. In addition, patients with manifest renal disease are considered at higher risk for the COVID-19 than healthy population due to the often-significant immunosuppressive pharmacotherapy that might be a part of various nephropathy treatment regimens.
The role of epoxyeicosatrienoic acids in blood pressure and renal function regulation in the experimental models of hypertension
Honetschlägerová, Zuzana ; Čertíková-Chábová, Věra (advisor) ; Zicha, Josef (referee) ; Maxová, Hana (referee)
Introduction: Epoxyeicosatrienoic acids (EETs) are converted by the enzyme soluble epoxid hydrolase (sEH) to the biologically inactive dihydroxyeicosatrienoic acids (DHETs). EETs are significantly involved in the control of blood pressure, they influence vascular tone and renal transport mechanism. sEH inhibitor reduce blood pressure by increasing the bioavailability of EETs in many models of hypertension. Aim of the study: To determine that sEH inhibitor decreases blood pressure and improves the renal function during the development of malignant hypertension in transgenic rats after the induction of the mouse renin gene. Methods: Hypertension in Cyp1a1-Ren-2 transgenic rats was induced through a dietary administration of the natural xenobiotic indole-3-carbinol (I3C, 0.3 %) for 3 and 11 days. I3C activates the renin gene. At the same time, during a three-day induction of hypertension, the inhibitor of nitric oxide synthase L-NAME (600 mg/l) was administered in drinking water. The sEH inhibitor c-AUCB was given in drinking water at a dose of 13 or 26 mg/l, starting 48 hours before the initiation of I3C and L-NAME administration. Radiotelemetric measurement of blood pressure was performed and renal excretory parameters were monitored in the conscious animals. The effects on renal hemodynamics and...
The role of arachidonic acid metabolites via cytochrome P-450 in the pathogenesis of hypertension
Čertíková-Chábová, Věra ; Tesař, Vladimír (advisor) ; Wilhelm, Jiří (referee) ; Štípek, Stanislav (referee)
Background: 20-HETE and EETs, metabolites derived from arachidonic acid by cytochrome P-450 (CYP), are part of the effector mechanisms in the renin-angiotenzin-aldosterone system. They regulate vasoconstriction/ vasodilation and natriuresis and thus contribute to the regulation of blood pressure. Hypertensive rats transgenic for mouse Re-2 renin gene (TGR) are a good model for hypertension caused by a single gene and very suitable for the study of the role20-HETE and EETs in vivo. Hypothesis: Abnormal production and/or activity of 20-HETE and EETs contributes to the development and or/maintenance of high blood pressure in TGR. Materials and methods: Hypertensive TGR heterozygous males of various ages weres studied. Normotensive HanSD animals (the same genetic background without Ren-2 gene) were used as controls. Three complex studies were performed: Study 1: Chronic inhibition of CYP with non-selective inhibitors 1- aminobenzotriazol (ABT) and CoCl2 in young prehypertensive and adult hypertensive animals and respective controls. Study 2: Acute experiments with selective inhibitors N-metyl-sulfonyl- 12,12-dibromododec-11- enamide (DDMS) and N-metylsulfonyl-6-(2- propargyloxyfenyl)-hexamide MS-PPOH. Study 3: Chronic selective inhibition of 20-HETE production by DDMS and selective inhibition of EETs...

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