Effects of lipid peroxidation, ca2+ and adrenalin on the release of fatty acids from rabbit kidney cortex slices

1982 ◽  
Vol 713 (3) ◽  
pp. 688-691 ◽  
Author(s):  
Fujimoto Yohko ◽  
Shimizu Keizo ◽  
Enmi Kazuko ◽  
Fujita Tadashi
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Cortex Slices ◽  
Kidney Cortex Slices

Effect of osmotic shocks on rabbit kidney cortex slices

1983 ◽  
Vol 244 (6) ◽  
pp. F696-F705
Author(s):  
R. Gilles ◽  
C. Duchene ◽  
I. Lambert
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Regulation Mechanism ◽  
Kidney Slices ◽  
Regulation Process ◽  
Maximum Cell ◽  
Cortex Slices ◽  
Kidney Cortex Slices

Rabbit kidney cortex slices behave an osmometers when withstanding hyperosmotic or hyposmotic shocks of amplitude up to pi 1/pi 2 = 1.25. For hyposmotic shocks of amplitude larger than or equal to pi 1/pi 2 = 1.50, the maximum swelling achieved is less than what can be expected on the basis of the van't Hoff relation, thereby indicating that a volume regulation process is taking place. Volume regulation in kidney slices can be dissociated into two distinct phases. The first one, of swelling limitation, is very rapid and keeps maximum cell volume at values lower than expected when the tissue is considered as an osmometer. This phase is followed by a slow volume readjustment process during which volume progressively decreases towards control values. The major intracellular osmotic effector loss during both swelling limitation and volume readjustment is Na+. The overall volume regulation process is insensitive to furosemide, vanadate, and bumetanide. Swelling limitation is blocked by addition of ouabain. Contrary to what has been believed previously, there is, however, no need to implicate control of the activity of a ouabain-sensitive, Na+/K+ pump in the Na-dependent volume regulation mechanism.

Concentrative PAH transport by rabbit kidney slices in the absence of metabolic energy

1978 ◽  
Vol 235 (4) ◽  
pp. F278-F285 ◽  
Author(s):  
R. A. Podevin ◽  
E. F. Boumendil-Podevin ◽  
C. Priol
Keyword(s):  
Membrane Potential ◽  
Metabolic Energy ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Intracellular Metabolism ◽  
Specific Stimulation ◽  
Cortex Slices ◽  
Dependent Transport ◽  
Kidney Cortex Slices ◽  
Stimulation Of

Characteristics of para-aminohippurate (PAH) transport in the absence of intracellular metabolism were studied with Na+, K+-depleted and ouabain-poisoned rabbit kidney cortex slices. The imposition of a NaCl gradient (out to in) resulted in specific stimulation of PAH uptake. PAH accumulated against its concentration gradient when cell [Na+] was less than medium [Na+]. Conversely, renal cells extruded PAH when cell [Na+] exceeded medium [Na+]. Membrane potential measured with triphenylmethylphosphonium revealed that conditions which created an interior-positive membrane potential inhibited the Na+-dependent transport of PAH but caused stimulation of the Na+-independent component. Characteristics of the Na+-dependent PAH transport system in ouabain-poisoned slices were similar to those previously described in metabolically active tissues.

Isoprenaline-Induced Secretion of Active and Inactive Renin in Anaesthetized Rabbits and by Kidney Cortex Slices

1981 ◽  
Vol 61 (6) ◽  
pp. 679-684 ◽  
Author(s):  
H. K. Richards ◽  
A. R. Noble ◽  
K. A. Munday
Keyword(s):  
Time Course ◽  
Urine Volume ◽  
Renin Release ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Active Renin ◽  
Arterial Blood ◽  
Inactive Renin ◽  
Cortex Slices ◽  
Kidney Cortex Slices

1. The effect of the β-adrenoceptor agonist isoprenaline on the secretion of active and inactive renin was investigated in two preparations. 2. in ten urethane-anaesthetized rabbits isoprenaline, given as a renal artery infusion, had relatively minor effects on renal sodium excretion (increased) and systemic arterial blood pressure (decreased). Urine volume, potassium excretion, creatinine clearance and serum electrolytes were all unchanged. Plasma active and inactive renin both increased immediately and returned to basal values after ceasing the isoprenaline infusion. 3. No significant changes in either plasma renin activity or renal function were observed in a group of ten control animals. 4. The magnitude of the isoprenaline-induced changes in plasma active renin was similar to that in a previous study of frusemide diuresis, but the time course was quite different. Inactive renin disappeared from plasma during frusemide diuresis. 5. Renin release by rabbit kidney cortex slices was also studied. Isoprenaline, added to the incubation medium, caused a dose-related increase in active renin secretion, but inactive renin release remained unchanged. This is in marked constrast to a previous study where reducing [Na+] increased active renin and inhibited inactive renin output. 6. These data support our previous suggestion that activation of inactive renin is regulated by a sodium-sensitive intrarenal mechanism.

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