scholarly journals Renin release and lipid peroxidation by ascorbic acid in the renin granule fraction of rat kidney cortex.

1983 ◽  
Vol 33 (4) ◽  
pp. 803-810
Author(s):  
Yasuo MATSUMURA ◽  
Toshikatsu SHIMIZU ◽  
Yukihiro OHNO ◽  
Nobuaki MIYAWAKI ◽  
Shiro MORIMOTO
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Rat Kidney ◽  
Renin Release ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Granule Fraction

scholarly journals RENIN RELEASE AND LIPID PEROXIDATION BY ASCORBIC ACID IN THE RENIN GRANULE FRACTION OF RAT KIDNEY CORTEX

1983 ◽  
Vol 33 (4) ◽  
pp. 803-810
Author(s):  
Yasuo MATSUMURA ◽  
Toshikatsu SHIMIZU ◽  
Yukihiro OHNO ◽  
Nobuaki MIYAWAKI ◽  
Shiro MORIMOTO
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Rat Kidney ◽  
Renin Release ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Granule Fraction

RENIN SECRETION IN VITRO FROM RAT KIDNEY CORTEX SLICES

1969 ◽  
Vol 60 (3) ◽  
pp. 550-554 ◽  
Author(s):  
Lj. Božović ◽  
S. Efendić
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Active Mechanism ◽  
Cortex Slices ◽  
Kidney Cortex Slices

ABSTRACT A method for in vitro studies of renin release is described. Kidney cortex slices taken from control rats and rats stimulated to release renin were incubated with and without glucose. Renin release from the slices to a large extent was glucose-dependent. This result supports the hypothesis of an active mechanism of renin secretion.

Inhibitory Role of Ca2+ in the Control of Renin Secretion: A Study Using Supervised Dispersed Rat Renal Cortical Cells

1989 ◽  
Vol 77 (3) ◽  
pp. 273-279 ◽  
Author(s):  
Karen Pardy ◽  
B. C. Williams ◽  
A. R. Noble
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Cortical Cells ◽  
Rat Kidney Cortex ◽  
Cyclic Monophosphate ◽  
Cortex Cell ◽  
The Mean

1. The role of Ca2+ in the control of renin release was investigated using a collagenase-dispersed rat kidney cortex cell preparation. 2. Superfusion with a series of low [Ca2+] buffers in either ascending or descending order of concentration increased renin release. Exposure to 0.06 mmol/l Ca2+ increased release by 120% (P < 0.001) when presented as the first buffer in ascending order of concentration and by 79% (P < 0.001) when presented as the fourth and last in a series of descending order. 3. The Ca2+ entry blocking drug diltiazem in a range of concentrations increased renin release and at 10−5 mol/l diltiazem the mean stimulation was 35% (P < 0.01). 4. 8-(N,N-Diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) reduces the release of Ca2+ from intracellular stores and, studied over a range of concentrations, this compound increased renin release. At 10−5 mol/l TMB-8 the mean increase was 44% (P < 0.001). 5. None of these experimental manipulations, low [Ca2+], diltiazem or TMB-8, had any effect on the release of adenosine 3′:5′-cyclic monophosphate into the cell superfusate, indicating that a decrease in intracellular [Ca2+] increases renin release by a mechanism which is independent of changes in adenosine 3′:5′-cyclic monophosphate production. 6. Effects of low [Ca2+], diltiazem and TMB-8 on renin secretion were all shown to be reversible when superfusion with control buffer was resumed.

scholarly journals Identification of metabolic pathways of the lipid peroxidation product 4-hydroxynonenal by mitochondria isolated from rat kidney cortex

FEBS Letters ◽  
1994 ◽  
Vol 352 (1) ◽  
pp. 84-86 ◽  
Author(s):  
Oliver Ullrich ◽  
Tilman Grune ◽  
Wolfgang Henke ◽  
Herrmann Esterbauer ◽  
Werner G. Siems
Keyword(s):  
Lipid Peroxidation ◽  
Metabolic Pathways ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Lipid Peroxidation Product ◽  
Rat Kidney Cortex ◽  
Peroxidation Product

scholarly journals Increase of Na/Pi-cotransport encoding mRNA in response to low Pi diet in rat kidney cortex.

1994 ◽  
Vol 269 (9) ◽  
pp. 6637-6639
Author(s):  
A. Werner ◽  
S.A. Kempson ◽  
J. Biber ◽  
H. Murer
Keyword(s):  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex

Acute lead exposure induces renal haeme oxygenase-1 and decreases urinary Na excretion

2003 ◽  
Vol 22 (5) ◽  
pp. 237-244 ◽  
Author(s):  
Hilda Vargas ◽  
Carlos Castillo ◽  
Francisco Posadas ◽  
Bruno Escalante
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Renal Function ◽  
Lead Exposure ◽  
Lead Acetate ◽  
Single Injection ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Tin Protoporphyrin ◽  
Pb Exposure

The effects of acute lead exposure on renal function, lipid peroxidation and the expression of haeme oxygenase (HO) in rat kidney were determined. A single injection of lead acetate (50 mg Pb/kg) was given to rats. Changes in renal function, characterized by a significant reduction in the Na excretion was observed six hours after Pb exposure; this effect persisted for 24 hours. TBARS levels increased in kidney cortex 24 hours after Pb administration. In kidney cortex, Pb exposure affected the expression of HO-1, a renal protein associated with oxidative stress. HO-1 mRNA increased 2.3-fold, three hours after Pb administration and remained increased for six, 12 and 24 hours. HO enzymatic activity and HO-1 protein increased six and three hours after Pb administration, respectively, and remained increased at 24 hours. HO inhibition by tin-protoporphyrin, potentiated Pb-induced increase in TBARS and prevented the Pb-induced reduction in Na excretion. Our data suggest that Pb may be acting through the generation of oxidant products and induction of HO.

Cytochrome P-450K of rat kidney cortex microsomes: Further studies on its interaction with fatty acids

1973 ◽  
Vol 158 (2) ◽  
pp. 597-604 ◽  
Author(s):  
Åke Ellin ◽  
Sten Orrenius ◽  
Åke Pilotti ◽  
Carl-Gunnar Swahn
Keyword(s):  
Fatty Acids ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex
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