Regulation of Urine Flow and Solute Excretion During Acute Acidosis Induced by Loading With Strong Mineral Acids in Hydropenic Dogs

1955 ◽  
Vol 181 (3) ◽  
pp. 616-624 ◽  
Author(s):  
William A. Brodsky
Keyword(s):  
Urine Flow ◽  
Mineral Acids ◽  
Solute Excretion

On the interaction of calcium, sodium, and water transport in the diuresing kidney

1968 ◽  
Vol 46 (2) ◽  
pp. 275-280 ◽  
Author(s):  
O. Schück ◽  
J. H. Cort
Keyword(s):  
Renal Function ◽  
Linear Relation ◽  
Filtration Rate ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Osmotic Diuresis ◽  
Anesthetized Dogs ◽  
Permeability For Water ◽  
Solute Excretion ◽  
Tubular Permeability

Diuresis was induced in cats by infusion of 3% glucose in 10% ethanol. When urine flow had stabilized at high levels a solution of the Ca salt of ethylenediaminetetraacetate (Na2CaEDTA) was infused as a control for the effect of the EDTA molecule on renal function. The infusion was then changed over to the same molar rate of Na2EDTA, which resulted in a 30% decrease in serum Ca levels. Ca was then repleted rapidly as CaCl2 given intravenously, and the infusion was shifted back to Na2CaEDTA. The decrease in extracellular Ca concentration was associated with a significant antidiuresis. In further experiments on anesthetized dogs, osmotic diuresis was induced either by (a) infusion of hyperosmotic mannitol solutions, which were then shifted over to hypertonic NaCl, or (b) the same solutions in reverse order. Ca excretion correlated in linear fashion with Na excretion, but not with total solute excretion or with filtration rate. When Ca was added to the mannitol infusion, Na excretion increased in linear relation to Ca. It is suggested that Ca (a) decreases tubular permeability for water reabsorption and (b) decreases Na reabsorption, while Na (c) decreases Ca reabsorption. Mechanisms a and b would appear to involve membrane transport directly in the proximal tubule.

Renal function in water snakes

1962 ◽  
Vol 203 (6) ◽  
pp. 995-1000 ◽  
Author(s):  
S. J. LeBrie ◽  
I. D. W. Sutherland
Keyword(s):  
Tubular Secretion ◽  
Urine Flow ◽  
Urinary Concentration ◽  
Clearance Ratio ◽  
Creatinine Concentration ◽  
Plasma Creatinine Concentration ◽  
Tenfold Increase ◽  
Solute Excretion ◽  
Water Snakes ◽  
Filtered Load

Electrolyte and osmolar concentrations of ureteral urine were compared with serum in several species of water snakes. Hyperosmotic urine was never observed, even after 48 hr of water deprivation. This finding is consistent with the countercurrent theory which precludes urinary concentration when Henle's loops are absent, as in reptilian kidneys. The creatinine/inulin clearance ratio may exceed 2.0, suggesting tubular secretion of creatinine. Tubular secretion is further suggested by the fact that the clearance ratio approaches unity when plasma creatinine concentration is elevated. Variations in glomerular activity are reflected in urine flow in snakes as shown by a direct relationship between clearance of inulin (GFR) and urine flow In snakes solute excretion is dependent on an increase in functional tubular population, with a concomitant increase in filtered load and not a decrease in tubular solute reabsorption. Evidence for this concept is presented and indicates that, over a tenfold increase in GFR, snakes continue to excrete about the same per cent of their filtered load. Water reabsorption, on the other hand, appears to be similar in character to that seen in higher vertebrates. Proximally, it appears to be dependent on solute reabsorption ("obligatory"), whereas distally it is influenced by ADH ("facultative").

Urinary pH as a determinant of prostaglandin E2 excretion by the conscious rat

1984 ◽  
Vol 66 (6) ◽  
pp. 675-681 ◽  
Author(s):  
J. Haylor ◽  
C. J. Lote ◽  
A. Thewles
Keyword(s):  
Prostaglandin E2 ◽  
Isotonic Saline ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Urine Ph ◽  
Conscious Rat ◽  
Conscious Rats ◽  
Positive Linear Correlation ◽  
Solute Excretion ◽  
Oral Sodium

1. The urinary excretion of prostaglandin E2 (PGE2) was measured in conscious rats under conditions which produced either acid or alkaline urine, but similar change in fluid and solute excretion. 2. Oral isotonic saline increased both urine flow and sodium excretion but did not alter urinary PGE2 output (which remained constant at 80 pmol/3 h per rat) or urine pH (6.2). 3. When the urine was made alkaline (pH 7.8) by oral sodium bicarbonate or carbonate, urinary PGE2 was approximately 3-fold greater (P<0.00l) than the control (pH6.2). The urine flow and sodium output were also increased. 4. When the urine was made acidic (pH 5.7) by oral ammonium chloride, urinary PGE, excretion was reduced (P<0.01) to approximately half the control output. The urine flow and sodium output increased. 5. Within a group of 12 rats receiving oral isotonic saline a positive linear correlation coefficient (P<0.002) was established between urine pH and PGE2 excretion. 6. The results indicate that urine pH may be a determinant of PGE2 excretion in unrestrained, conscious rats. It seems likely that this effect of pH is mediated by a change in the passive reabsorption of PGE, in the distal nephron, although alternative explanations such as altered tubular secretion or synthesis cannot be categorically excluded.

Unilateral renal ischaemia in the rat: Effect of contralateral nephrectomy and intrarenal flush with phosphate-buffered sucrose

1988 ◽  
Vol 74 (3) ◽  
pp. 261-268 ◽  
Author(s):  
O. S. Ferwana ◽  
S. C. Pirie ◽  
D. J. Potts
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Kidney Tissue ◽  
Urine Flow ◽  
Compensatory Response ◽  
Contralateral Kidney ◽  
Renal Ischaemia ◽  
Ischaemic Damage ◽  
Solute Excretion

1. This study examined whether the severity of acute renal failure seen within 4 h of a 45 min period of unilateral occlusion of the renal pedicle could be reduced by removal of the contralateral healthy kidney and/or intrarenal flush with a phosphate-buffered sucrose (PBS50) solution. 2. After ischaemia, unflushed kidneys became oliguric and isosthenuric, with a fall in inulin clearance (Cin) to 0.1% of the pre-ischaemic value. Removal of the healthy contralateral kidney upon release of the occlusion caused no improvement in immediate post-ischaemic function. 3. Intrarenal flush with 1.5 ml of PBS50 resulted in a significantly improved post-ischaemic Cin, with increased urine flow rate and solute excretion; urine was also concentrated. 4. Protection of renal function against ischaemic damage was seen only when kidney tissue remained blood-free and exposed to PBS50 throughout the period of ischaemia, and when the speed of flush was similar to the expected renal blood flow (6 ml/min). Protection did not depend upon the presence or absence of the contralateral kidney. 5. The study also showed that functional removal of one kidney, either by pedicle occlusion or nephrectomy, caused an immediate rise in solution excretion from the contralateral kidney, but Cin remained unchanged. Unflushed severely damaged kidneys showed no compensatory response to unilateral nephrectomy, whereas kidneys flushed with PBS50 exhibited increases in solute excretion similar to those seen in healthy non-ischaemic kidneys.

Central effects of endothelin-1 on vasopressin release, blood pressure, and renal solute excretion

1992 ◽  
Vol 262 (6) ◽  
pp. E856-E862 ◽  
Author(s):  
T. Yamamoto ◽  
T. Kimura ◽  
K. Ota ◽  
M. Shoji ◽  
M. Inoue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Nervous Activity ◽  
Urine Flow ◽  
Vasopressin Release ◽  
Central Effects ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Solute Excretion

To assess central effects of endothelin-1 (ET-1) on plasma arginine vasopressin (AVP), plasma atrial natriuretic peptide (ANP), blood pressure, heart rate, and renal solute excretion, ET-1 dissolved in the artificial cerebrospinal fluid was infused intracerebroventricularly (icv) at a dose of either 0.35 ng.kg-1.min-1 (0.14 pmol; LET) or 3.5 ng.kg-1.min-1 (1.4 pmol; HET) for 45 min in conscious rats. In the control study, ET-1 was omitted from the vehicle. Moreover, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-O-methyl-tyrosine]AVP (TMeAVP), a V1-blocker, and prazosin, an alpha 1-blocker, were peripherally administered. In the LET group, mean arterial blood pressure (MABP) increased without any changes in heart rate, plasma AVP and ANP, and renal solute excretion. In the HET group, MABP markedly increased with rises in plasma AVP and ANP, but urine flow, urinary osmolality, and urinary Na and K excretion decreased. TMeAVP attenuated the pressor response to ET-1, abolished rises in plasma ANP, and partially restored falls in urine flow. Prazosin after TMeAVP obviated the pressor response to ET-1. In the control, these parameters did not change, except for an increase in urinary solute excretion. These results showed that icv ET-1 stimulates the sympathetic nervous activity and plasma AVP, leading to increased blood pressure and renal vasoconstriction, with a reduction in renal water and electrolyte excretion.

Relative roles of glomerular filtration and tubular reabsorption in denervation diuresis

1962 ◽  
Vol 202 (4) ◽  
pp. 777-780 ◽  
Author(s):  
William D. Blake
Keyword(s):  
Glomerular Filtration ◽  
Filtration Rate ◽  
Tubular Reabsorption ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Reabsorptive Capacity ◽  
Standard Procedures ◽  
Total Filtration ◽  
Proximal Tubular ◽  
Solute Excretion

Experiments have been carried out on anesthetized, laparotomized dogs in which urine samples were collected from both kidneys after acute denervation of one. Renal functions were estimated by standard procedures with creatinine clearance (CCr) as an index of glomerular filtration rate. Urine flow and solute excretion were greater from the denervated kidney (D) than from the innervated kidney (I) under all conditions of solute diuresis. The magnitude of denervation diuresis, D/I for urine flow, was directly related to the relative excess of electrolyte excretion on the denervated side, D/I for electrolyte excretion rate. D/I for electrolyte excretion was not correlated with D/I for CCr and remained above 100% in all experiments despite a fall of D/I for CCr below 100% in 10 of 30 comparisons. Since excessive electrolyte excretion by the denervated kidney could not be explained by greater total filtration rate, it was reaffirmed that denervation caused a defect in proximal tubular reabsorption of sodium, either by decreased reabsorptive activity of all tubules or by redistribution of filtration toward tubules of lesser reabsorptive capacity.

Sign in / Sign up

Export Citation Format

Share Document