Renal sodium reabsorption and oxygen consumption after unilateral splanchnicotomy in the dog

1974 ◽  
Vol 349 (4) ◽  
pp. 359-367 ◽  
Author(s):  
L. Szalay ◽  
P. Bencs�th ◽  
L. Tak�cs
Keyword(s):  
Oxygen Consumption ◽  
Sodium Reabsorption ◽  
Renal Sodium Reabsorption

Effects of cyanide, Q0, and dinitrophenol on renal sodium reabsorption and oxygen consumption

1964 ◽  
Vol 206 (6) ◽  
pp. 1327-1332 ◽  
Author(s):  
M. Fujimoto ◽  
F. D. Nash ◽  
R. H. Kessler
Keyword(s):  
Oxygen Consumption ◽  
Total Dose ◽  
Coenzyme Q ◽  
Atp Synthesis ◽  
Metabolic Inhibitors ◽  
Sodium Reabsorption ◽  
Major Fraction ◽  
Variable Effect ◽  
Anesthetized Dogs ◽  
Renal Sodium Reabsorption

Effects on sodium reabsorption and oxygen consumption of the renal arterial injection of three metabolic inhibitors were studied by unilateral clearance techniques in anesthetized dogs. In control studies, 21.5 ± 2.3 mEq sodium were reabsorbed per millimole oxygen consumed within a range of sodium reabsorption of from 2 to 9 mEq/min. A total dose of 10–4 m cyanide depressed both sodium reabsorption and oxygen consumption in the injected kidney. Administration of 10–4 m Q0, the quinone nucleus of coenzyme Q, reduced sodium reabsorption and had a variable effect on O2 consumption. Dinitrophenol, in a total dose of 10–3 m, increased oxygen consumption without affecting the per cent of filtered sodium that was reabsorbed. The resultant Na:O2 ratios were 12:1. We conclude that the major fraction of O2 consumption energizes sodium reabsorption in the kidney perhaps via the classic route of ATP synthesis and hydrolysis. However, all three compounds used in this study would be predicted to decrease renal ATP concentrations. Yet only cyanide and Q0 decreased sodium reabsorption. Energy for sodium movement may come directly from oxidative metabolism bypassing synthesis and breakdown of ATP.

Effects of Chlormerodrin, p-Chloromercuribenzoate and Dichlorphenamide on Renal Sodium Reabsorption and Oxygen Consumption

Nephron ◽  
1964 ◽  
Vol 1 (4) ◽  
pp. 221-229 ◽  
Author(s):  
R.H. Kessler ◽  
S.W. Weinstein ◽  
F.D. Nash ◽  
M. Fujimoto
Keyword(s):  
Oxygen Consumption ◽  
Sodium Reabsorption ◽  
Renal Sodium Reabsorption

Single-nephron function and renal oxygen consumption during rapid volume expansion

1976 ◽  
Vol 231 (4) ◽  
pp. 1166-1172 ◽  
Author(s):  
SW Weinstein ◽  
J Szyjewicz
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Ringer Solution ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Renal Oxygen Consumption ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Renal Sodium Reabsorption

Isotonic volume expansion reduces net filtrate reabsorption in the proximal tubule while increasing it in Henle's loop. To determine the role oxidative metabolism plays in these processes, experiments were performed on rats initially hydropenic and then rapidly volume expanded with isotonic Ringer solution. Whole-kidney sodium reabsorption, oxygen consumption, and single-nephron function were measured simultaneously. During volume expansion, net renal sodium reabsorption increased concomitantly with a fall in oxygen consumption and a reduction in proximal tubular absolute filtrate reabsorption. The increase in quantity of nonreabsorbed filtrate delivered into the loop of Henle greatly exceeded the amount excreted in the urine. Thus, filtrate reabsorption by the distal nephron segments increased. These data provide evidence that acute volume expansion reduces oxygen-dependent active solute transport in the proximal tubule. The increase noted in distal nephron sodium reabsorption appears nonoxygen dependent, energized by anaerobic glycolysis or occurring passively.

Renal sodium reabsorption, oxygen consumption, and gamma-glutamyltransferase excretion in the postischemic rat kidney

1985 ◽  
Vol 248 (6) ◽  
pp. F804-F809 ◽  
Author(s):  
D. Herminghuysen ◽  
C. J. Welbourne ◽  
T. C. Welbourne
Keyword(s):  
Oxygen Consumption ◽  
Brush Border ◽  
Rat Kidney ◽  
Renal Plasma Flow ◽  
Control Level ◽  
Sodium Reabsorption ◽  
Marker Enzyme ◽  
Gamma Glutamyltransferase ◽  
Renal Oxygen Consumption ◽  
Renal Sodium Reabsorption

The effect of 30 min of renal artery occlusion on renal sodium reabsorption, oxygen consumption, and brush border integrity was studied in the immediate 1-h reflow period. Rats were studied using clearance and renal extraction measurements. Glomerular filtration rate and renal plasma flow were measured over four consecutive 15-min periods; renal venous samples were drawn via an indwelling catheter. Renal oxygen consumption (QO2) was calculated from renal blood flow, corrected for urine flow, and from blood oxygen content measured with a fuel cell analyzer. Brush border integrity was assessed by the excretion of the brush border marker enzyme gamma-glutamyltransferase as well as by morphologic observation. Ischemia induced a 10-fold rise in fractional sodium excretion in the initial 0- to 15-min period, rose to 20-fold during the subsequent two periods, 15-45 min, and then returned to the initial reflow period level. The progressive deterioration of renal function with reflow could not be attributed to an increase in the filtered Na+ load. Rather, Na+ reabsorption appeared to be related to the presence of intact brush borders at 0-15 min, their removal from the luminal surface between 15 and 45 min, and their return at 60 min of reflow. Renal QO2 was coupled to Na+ reabsorption in the initial 15-min and final 45- to 60-min reflow periods. However QO2 was significantly increased over the control level at 30-45 min of reflow. The results point to a significant role of brush border uptake in the development of functional impairment following renal ischemia and suggest that the associated rise in renal O2 consumption may be coupled to the reparation of this organelle.

Insulin Effect on Renal Sodium Reabsorption in Adolescent Offspring of Essential Hypertensive Parents

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1089-1092 ◽  
Author(s):  
B. Grunfeld ◽  
M. Gimenez ◽  
M. Balzaretti ◽  
L. Rabinovich ◽  
M. Romo ◽  
...  
Keyword(s):  
Sodium Reabsorption ◽  
Insulin Effect ◽  
Adolescent Offspring ◽  
Renal Sodium Reabsorption

Stimulation of renal sodium reabsorption by angiotensin II

1977 ◽  
Vol 232 (4) ◽  
pp. F298-F306 ◽  
Author(s):  
M. D. Johnson ◽  
R. L. Malvin
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Filtration Fraction ◽  
Water Diuresis ◽  
Urinary Osmolality ◽  
Anesthetized Dogs ◽  
Renal Sodium Reabsorption

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.

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