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1
Content available remote

The role of peroxisome-proliferator-activating receptor gamma agonists: rosiglitazone and 15-deoxy-delta12,14-prostaglandin J2 in chronic experimental cyclosporine A-induced nephrotoxicity

100%
Korolczuk A., Maciejewski M., Smolen A., Dudka J., Czechowska G., Widelska I.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 6
2
Content available remote

Urocortin 2 in patients with hypertension treated with angiotensin converting enzyme inhibitors or angiotensin receptor blockers

100%
Walczewska J., Siga O., Dziezga-Grudnik A., Krolczyk J., Wizner B., Wolkow P. P., Borys A., Kolton-Wroz M., Gryglewska B., Grodzicki T.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 2
3
Content available remote

Spironolactone, but not enalapril, potentiates hypoxia-inducible factor-1alpha and Ets-1 expression in newborn rat kidney

80%
Yim H. E., Kim J. H., Yoo K. H., Bae I. S., Jang G. Y., Hong Y. S., Lee J. W.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 1
73-81
Hypoxia is regarded as an important physiological factor that controls nephrogenesis. We investigated whether the renin-angiotensin-aldosterone system (RAAS) affects hypoxia-related target genes in developing kidneys. Newborn rat pups were treated with enalapril (30 mg/kg/d) or spironolactone (200 mg/kg/d) for 7 days. Tissue hypoxia was assessed by the uptake of a hypoxyprobe-1, pimonidazole (200 mg/kg), and the expression of hypoxia-responsive genes. In the enalapril group, hypoxia-inducible factor (HIF)-1, HIF-2, and Ets-1 protein expression were not changed, compared to the control group. In the spironolactone group, HIF-1 and Ets-1 protein expression were significantly increased by immunoblots and immunohistochemistry, whereas HIF-2 protein expression was not changed, compared to the control group. In the enalapril group, the immunoactivity of pimonidazole was not significantly different from that of the controls. However, in the spironolactone group, pimonidazole staining demonstrated that the cortex and medulla underwent severe hypoxia. In summary, our data showed that aldosterone inhibition in the developing kidney augmented the hypoxic responses, and up-regulated the expression of key mediators of hypoxia including HIF-1 and Ets-1. Angiotensin II inhibition did not affect hypoxia-related alterations in the developing kidney. The components of RAAS may differentially modulate renal hypoxia and its related target genes in the developing rat kidney.
4

Ramipril affects hydrogen sulfide generation in mouse liver and kidney

80%
Wilinski B., Wilinski J., Somogyi E., Goralska M., Piotrowska J.
Folia Biologica
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2010
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tom 58
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nr 3-4
177-180
5
Content available remote

The expression of the renin-angiotensin-aldosterone system in the skin and its effects on skin physiology and pathophysiology

80%
Aleksiejczuk M., Gromotowicz-Poplawska A., Marcinczyk N., Przylipiak A., Chabielska E.
Journal of Physiology and Pharmacology
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2019
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tom 70
|
nr 3
6

Renin - angiotensin - aldosterone system versus osmotic pressure of blood plasma in calves in the neonatal period

80%
Ozgo M.
Electronic Journal of Polish Agricultural Universities. Series Veterinary Medicine
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2001
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tom 04
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nr 2
7
Content available remote

Central TNF-alpha elevates blood pressure and sensitizes to central pressor action of angiotensin II in the infarcted rats

80%
Zera T., Ufnal M., Szczepanska-Sadowska E.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 8
8

Gene polymorphisms of the renin-angiotensin-aldosterone system and essential arterial hypertension in childhood

80%
Petrovic D., Bidovec M., Peterlin B.
Folia Biologica
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2002
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tom 50
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nr 1-2
9
Content available remote

Nifedipine inhibits the hypoxia-induced decrease in plasma renin activity in conscious dogs

80%
Hohne C., Arntz E., Krebs M. O., Boemke W., Kaczmarczyk G.
Journal of Physiology and Pharmacology
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2003
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tom 54
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nr 2
Acute hypoxia induces a decrease in plasma renin activity (PRA), mediated, e.g., by an increase in adenosine concentration, calcium channel activity, or inhibition of ATP-sensitive potassium channels. The decrease in PRA results in a decrease in angiotensin II (AngII) and plasma aldosterone concentration (PAC). This study investigates whether these hypoxia-induced mechanisms can be inhibited by the L-type voltage-dependent calcium channel antagonist nifedipine. Eight conscious, chronically tracheotomized dogs received a low sodium diet (0.5 mmol Na·kg body wt-1·day-1). The dogs were studied twice in randomized order, either with nifedipine infusion (1.5 µg·kg body wt-1·min-1, Nifedipine) or without (Control). The dogs were breathing spontaneously: first hour, normoxia [inspiratory oxygen fraction (FiO2)=0.21]; second and third hour hypoxia (FiO2=0.1). In Controls, PRA (6.8±0.8 vs. 3.0±0.5 ngAngI·ml-1·min-1), AngII (13.3±1.9 vs. 7.3±1.9 pg/ml), and PAC (316±50 vs. 69±12 pg/ml) decreased during hypoxia (P<0.05). In Nifedipine experiments, PRA (6.5±0.9 vs. 10.5±2.4 ngAngI·ml-1·min-1) and AngII (14±1.1 vs. 18±3.9 pg/ml) increased during hypoxia, whereas the decrease in PAC (292±81 vs. 153±41 pg/ml) was blunted (P<0.05). These results foster the idea that the hypoxia-induced decrease in PRA involves L-type calcium channel activity.
10

Jak osiągnąć równowagę u pacjentów z chorobą układu sercowo-naczyniowego i chorobą nerek?

61%
Cook A. K., Saunders A. B.
Weterynaria po Dyplomie
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2019
|
tom 20
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nr 6
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