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.

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.

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 DIRECT COUNTING AND SIZING OF MITOCHONDRIA IN SOLUTION

1972 ◽  
Vol 54 (2) ◽  
pp. 325-345 ◽  
Author(s):  
Adrian R. L. Gear ◽  
Jana M. Bednarek
Keyword(s):  
Electron Microscopy ◽  
Rat Liver ◽  
Rat Kidney ◽  
Mitochondrial Protein ◽  
Kidney Cortex ◽  
Rat Liver Mitochondria ◽  
Particle Volume ◽  
Drug Induced ◽  
Rat Kidney Cortex ◽  
The Mean

Resistive particle counting has been developed for the accurate sizing and counting of mitochondria in solution. The normal detection limit with a 30 µ aperture is 0.48 µ diameter, or 0.056 µ3 particle volume The mean volume of rat liver mitochondria was 0.42 µ3 or 0.93 µ in diameter. The average value for numbers of particles per milligram of mitochondrial protein was 4.3 x 103, and per gram of rat liver was about 11 x 1010. These values compare satisfactorily with those derived by light microscopy and electron microscopy. The mean volume for mitochondria from rat heart was 0 60 µ3 and from rat kidney cortex, 0.23 µ3. These values agree within 15% of those determined by electron microscopy of whole tissue. Mitochondrial fragility and contaminating subcellular organelles were shown to have little influence on the experimentally determined size distributions The technique may be applied to rapid swelling studies, as well as to estimations of the number and size of mitochondria from animals under different conditions such as liver regeneration and hormonal, pathological, or drug-induced states Mitochondrial DNA, RNA, cytochrome c-oxidase, cytochrome (a ÷ a3), and iron were nearly constant per particle over large differences in particle size. Such data may be particularly valuable for biogenesis studies and support the hypothesis that the net amount per particle of certain mitochondrial constituents remains constant during mitochondrial growth and enlargement

Effect of bicarbonate on glutamine and glutamate metabolism by rat kidney cortex mitochondria

1985 ◽  
Vol 249 (4) ◽  
pp. F573-F581
Author(s):  
R. C. Scaduto ◽  
A. C. Schoolwerth
Keyword(s):  
Rat Kidney ◽  
Competitive Inhibitor ◽  
Kidney Cortex ◽  
Mitochondrial Enzymes ◽  
Glutamate Metabolism ◽  
Bicarbonate Buffer ◽  
Rat Kidney Cortex ◽  
Glutamate Oxalacetate Transaminase ◽  
Stimulation Of

Isolated rat kidney cortex mitochondria were incubated at pH 7.4 in the presence or absence of a CO2/bicarbonate buffer (28 mM) to investigate the pH-independent role of bicarbonate on glutamine and glutamate metabolism. Changes in the concentration of key intermediates and products during the incubations were used to calculate metabolite flux rates through specific mitochondrial enzymes. With 1 mM glutamine and 2 mM glutamate as substrates, bicarbonate caused an inhibition of glutamate oxalacetate transaminase flux and a stimulation of glutamate deamination. The same effects were also produced with addition of either aminooxyacetate or malonate. These effects of bicarbonate were prevented when 0.2 mM malate was included as an additional substrate. Bicarbonate ion was identified as a potent competitive inhibitor of rat kidney cortex succinate dehydrogenase. These results indicate that aminooxyacetate, malonate, and bicarbonate all act to stimulate glutamate deamination through a suppression of glutamate transamination, and that the control by transamination of glutamate deamination is due to alterations in alpha-ketoglutarate metabolism. In contrast, in mitochondria incubated with glutamine in the absence of glutamate, bicarbonate was found to inhibit glutamate dehydrogenase flux. This effect was found to be due in part to the lower intramitochondrial pH observed in incubations with bicarbonate. These findings indicate that bicarbonate ion, independent of pH, may have an important regulatory role in renal glutamine and glutamate metabolism.

The role of calcium in the control of renin release from the isolated rat kidney

1980 ◽  
Vol 58 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Alexander G. Logan ◽  
Alice Chatzilias
Keyword(s):  
Rat Kidney ◽  
Experimental Period ◽  
Renin Secretion ◽  
Renin Release ◽  
Base Line ◽  
Isolated Perfused Kidney ◽  
Renal Vasoconstriction ◽  
Perfusate Flow ◽  
Perfused Kidney

The effect of verapamil and manganese on isoproterenol- and glucagon-evoked renin secretion and on norepinephrine-induced renal vasoconstriction was studied in the isolated perfused kidney. Results for renin secretion and perfusate flow rates were expressed as the ratio of the average of the two values which deviated furthest from base line during the experimental period to the average of two control values determined at the beginning of each experiment. Norepinephrine significantly reduced (p < 0.001) the perfusate flow ratio to 0.35 ± 0.06 (mean ± SEM) without having any effect on renin secretion. During Ca2+-free perfusion, norepinephrine-induced renal vasoconstriction was completely abolished and concomitantly the renin secretion ratio increased significantly (p < 0.001) to 6.28 ± 1.24. Verapamil attenuated and manganese chloride abolished norepinephrine-induced renal vasoconstriction. Renin secretion increased significantly (p < 0.001) to 9.26 ± 1.79 and 9.92 ± 1.93 in the verapamil and manganese experiments, respectively. Verapamil and manganese themselves did not significantly alter renin secretion or perfusate flow and neither inhibited renin secretion induced by isoproterenol and glucagon. In conclusion, extracellular Ca2+ and net Ca2+ influx are prerequisites for norepinephrine to produce renal vasoconstriction and to inhibit renin release in the isolated perfused kidney. On the other hand, renin secretion evoked by isoproterenol and glucagon does not seem to require the movement of extracellular calcium into juxtaglomerular cells and it is speculated that the level of adenylate cyclase activity may be an important determinant of the rate of renin release.

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 PPARα Gene Expression in the Developing Rat Kidney: Role of Glucocorticoids

2001 ◽  
Vol 12 (6) ◽  
pp. 1197-1203
Author(s):  
FATIMA DJOUADI ◽  
JEAN BASTIN
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Culture Media ◽  
Rat Kidney ◽  
Fold Increase ◽  
Kidney Cortex ◽  
Peroxisome Proliferator ◽  
Rat Kidney Cortex

Abstract. The α isoform of peroxisome proliferator-activated receptor (PPARα), which is highly expressed in the kidney, can stimulate the expression of genes that are involved in fatty acid catabolism and therefore might be involved in the control of renal fatty acid β-oxidation. PPARα expression and its regulation in the immature kidney are not well documented. This study delineated the developmental pattern of PPARα expression in the rat kidney cortex and the medulla between postnatal days 10 and 30 and investigated the role of glucocorticoids in regulating PPARα expression. In the cortex, PPARα mRNA and protein increased 2- and 1.8-fold, respectively, from 10 to 21 d and then decreased 1.5- and 2.4-fold from 21 to 30 d. In the medulla, PPARα mRNA and protein increased continuously 3.3- and 2.4-fold, respectively. It is shown here that acute treatment by dexamethasone of 10-d-old rats precociously induced a 4- to 6-fold increase in PPARα mRNA and a 1.8-fold increase in protein within 6 h in each part of the kidney. Chronic injection of dexamethasone for 3 d also increased PPARα mRNA 3.8- and 2.2-fold in the cortex and the medulla, respectively, with a 1.5- and 2-fold increase in protein. Furthermore, adrenalectomy prevented the increases in PPARα mRNA and protein in both the cortex and the medulla between postnatal days 16 and 21, and these could be restored by dexamethasone treatment. Finally, with the use of an established renal cell line, it was shown that glucocorticoids stimulate gene expression of PPARα and of medium chain acyl-CoA dehydrogenase (MCAD, a PPARα target gene) 2- to 4-fold and 1.5-fold, respectively, and that addition of fatty acids in the culture media led to a 2.2-fold increase in MCAD mRNA. Altogether, these results demonstrated that glucocorticoids are potent regulators of PPARα development in the immature kidney and that these hormones act in concert with fatty acids to regulate MCAD gene expression in renal cells.

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