The renal response of sheep to feeding

Acute changes in renal excretion occurred when pen-fed sheep were given their daily feed. There was a reduction in the rate of urine flow and the concentration of the urine increased. During the oliguric phase, sodium and potassium excretion decreased whereas hydrogen ion excretion increased and caused acidification (pH 5–6) of the normally alkaline urine (pH 7–8). Renal clearances of inulin and PAH did not indicate that the urinary changes were due to altered renal haemodynamics. It is suggested that the observed renal response was a reflection of the sudden shift of extracellular fluid into the gut at the onset of feeding.

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Lack of Dependence of Urine Pco2 upon Reduction of Glomerular Filtration Rate in Alkalotic Dogs

Clinical Science ◽

10.1042/cs0520119 ◽

1977 ◽

Vol 52 (2) ◽

pp. 119-123

Author(s):

B. J. Stinebaugh ◽

T. H. Hostetter ◽

R. A. Peraino ◽

F. X. Schloeder ◽

W. N. Suki

Keyword(s):

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Filtration Rate ◽

Urine Flow ◽

Hydrogen Ion ◽

Alkaline Urine ◽

Ion Secretion ◽

Arterial Blood ◽

Excretion Rates ◽

Acute Changes

1. The Pco2 gradient between alkaline urine and arterial blood (U—B Pco2) is thought to depend primarily on distal hydrogen ion secretion. However, other variables affecting the U—B Pco2 include the urine flow rate, the urinary bicarbonate and phosphate excretion rates and the glomerular filtration rate. 2. In order to evaluate the effects of acute changes in these factors on the U—B Pco2, bicarbonate-loaded dogs with maximal U—B Pco2 values were subjected to either acute unilateral elevations of ureteral pressure or hypotension caused by nitroprusside infusion. The results demonstrate that acute reduction in the glomerular fiitration rate does not cause a decrease in the U—B Pco2 as long as the urinary concentrations of phosphate and bicarbonate do not decline. 3. Urinary concentrations of phosphate and bicarbonate appeared more important than their excretion rates in the maintenance of elevated U—B Pco2 values.

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Renal acidification in the hypothyroid rat. Evaluation by urinary CO2 tension

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y81-043 ◽

1981 ◽

Vol 59 (3) ◽

pp. 273-280 ◽

Cited By ~ 3

Author(s):

Ulrich F. Michael ◽

Jan Kelley ◽

Laurence A. Meeks ◽

Carlos A. Vaamonde

Keyword(s):

Intraperitoneal Injection ◽

Urine Flow ◽

Hydrogen Ion ◽

Renal Response ◽

Ion Secretion ◽

Phosphate Loading ◽

The Difference ◽

Excretion Rates ◽

Acid Loading ◽

Lower Urinary

We have previously demonstrated an abnormal renal response to chronic acid loading in the hypothyroid rat. The present study was designed to characterize further this defect by examining the renal response to bicarbonate loading. Hypothyroidism was induced by the intraperitoneal injection of Na131I and animals were studied 10 or more weeks thereafter under anesthesia and compared with their age-matched littermates. Inulin clearance of hypothyroid animals was lower and fractional urine flow and sodium excretion rates were higher than in the control rats. At the time of maximal urinary bicarbonate levels, the urine [Formula: see text] exceeded blood values [Formula: see text] by 41 ± 2 (mean ± SE) mmHg (1 mmHg = 133.322 Pa) in the controls and 25 ± 3 mmHg in the hypothyroid rats (p < 0.001). Although maximal urinary bicarbonate concentrations achieved during bicarbonate loading were lower in the hypothyroid animals, [Formula: see text] was consistently less than in controls when compared at similar urine bicarbonate concentrations. Thus, the difference in [Formula: see text] was not explained by lower urinary bicarbonate concentrations in the hypothyroid animals. Maximal [Formula: see text] during neutral phosphate loading was significantly less in the hypothyroid rats (38 ± 2 mmHg) than in the controls (68 ± 5 mmHg), p < 0.001, arguing against a gradient defect of distal hydrogen ion handling. These data indicate that hypothyroid rats exhibit an impairment of distal hydrogen ion secretion.

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Characterization of distal hydrogen ion secretion in acute respiratory alkalosis

AJP Renal Physiology ◽

10.1152/ajprenal.1978.235.3.f203 ◽

1978 ◽

Vol 235 (3) ◽

pp. F203-F208

Author(s):

J. T. Sehy ◽

M. K. Roseman ◽

J. A. Arruda ◽

N. A. Kurtzman

Keyword(s):

Respiratory Alkalosis ◽

Hydrogen Ion ◽

Distal Nephron ◽

Urine Ph ◽

Alkaline Urine ◽

Ion Secretion

The effect of acute respiratory alkalosis (ARA) on distal nephron H+ secretion was evaluated by measuring urine-to-blood (U-B) Pco2 in dogs with highly alkaline urine (urine pH greater than 7.8). ARA led to a significant decrease in U-B Pco2 and in urine HCO3 concentration; urine pH, however, increased significantly, indicating that the decrease in urine Pco2 was of greater magnitude than the decrease in urine HCO3 concentration. For any given urine HCO3 concentration urine Pco2 was lower (i.e., urine pH was higher) in ARA than in controls. Administration of tris(hydroxymethyl)aminomethane (Tris) during ARA resulted in a significant increase in U-B Pco2 to control values. In animals with moderately alkaline urine (urine pH 6.4--7.4) and high urine PO4 concentration, ARA resulted in a significant decrease in UB-Pco2 and urine PO4 concentrations. Neutral PO4 infusion in these dogs resulted in an increase in urine PO4 concentration and U-B Pco2 to control levels. These data demonstrate that ARA results in a significant decrease in U-B Pco2 that is not solely attributable to changes in urine HCO3 concentration. The observation that Tris and PO4 infusion during ARA raises U-B Pco2 to control levels suggests that the ability to secrete H+ is intact.

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Urine pH and the relationship between urine flow and urinary prostaglandin E excretion in the rat

Journal of Endocrinology ◽

10.1677/joe.0.1080247 ◽

1986 ◽

Vol 108 (2) ◽

pp. 247-253 ◽

Cited By ~ 4

Author(s):

J. Haylor ◽

C. J. Lote

Keyword(s):

Sodium Bicarbonate ◽

Ammonium Chloride ◽

Urine Flow ◽

Low Flow ◽

Common Mechanism ◽

Prostaglandin E ◽

Urine Ph ◽

Alkaline Urine ◽

Flow Dependency ◽

The Relationship

ABSTRACT The relationship between urine flow and urinary prostaglandin E (PGE) excretion was investigated at constant urine pH in the anaesthetized rat. The urine pH was maintained at approximately pH 6 or pH 8 by the intravenous infusion of either ammonium chloride or sodium bicarbonate respectively. Two distinct patterns in the relationship between PGE excretion and urine flow were observed. The first showed a fall in urinary PGE excretion as the urine flow increased over the low flow range of 2–5 ml/h, and was common to both experiments. The second relationship, however, showed a marked difference between the ammonium chloride and sodium bicarbonate experiments since: (a) in acidic urine (pH 6), PGE excretion increased (P < 0·002) with the urine flow, attaining a rate of 87± 6 pmol/h (n = 6) at the highest level of flow achieved (12 ml/h); (b) in alkaline urine (pH 8), PGE excretion was significantly (P < 0·01) higher but did not increase with urine flow, remaining constant at approximately 90 pmol/h (n = 6). The lack of any additive effect on urinary PGE excretion between increasing the urine flow and making the urine alkaline may be explained by both stimuli acting through a common mechanism, a concept which is consistent with the hypothesis that PGE may be reabsorbed in the distal nephron. The flow-dependency of urinary PGE excretion could therefore result from a reduction in reabsorption rather than the increase in passive secretion proposed previously. In addition, PGE excretion in alkaline urine may be a more appropriate index of renal PGE synthesis, since above a urine pH of 7·5 its excretion is independent of both urine pH and urine flow. J. Endocr. (1986) 108, 247–253

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Renal excretion of phosphate and calcium in parathyroidectomized starlings

AJP Renal Physiology ◽

10.1152/ajprenal.1977.233.2.f138 ◽

1977 ◽

Vol 233 (2) ◽

pp. F138-F144 ◽

Cited By ~ 2

Author(s):

N. B. Clark ◽

R. F. Wideman

Keyword(s):

Filtration Rate ◽

Renal Excretion ◽

Tubular Secretion ◽

Tubular Reabsorption ◽

Urine Flow ◽

Phosphate Homeostasis ◽

Calcium Clearance ◽

Parathyroid Extract ◽

Potassium Secretion ◽

Sodium And Potassium

Renal excretion patterns of calcium, phosphate, sodium, and potassium were studied in parathyroidectomized (PTX) and parathyroid extract (PTE)-injected PTX starlings. Sturnus vulgaris. Anesthetized birds (Equi-Thesin or Dial) were infused intravenously with 2.5% mannitol containing [14C]inulin. PTX caused significant hypocalcemia, hyperphosphatemia, increased relative calcium clearance (CCa/CIn), and decreased relative clearances of phosphate and potassium, but did not change the clearance of sodium. Glomerular filtration rate (GFR=CIn) and urine flow remained unchanged up to 2 h after PTX. PTE administration 3 h after PTX returned serum calcium and phosphate values to control levels and caused a transient (10-min) increase in GFR. Following PTE, the relative clearances of phosphate, sodium- and potassium increased, while that of calcium decreased significantly relative to the PTX levels. PTE caused net tubular secretion of phosphate, decreased tubular reabsorption of sodium and potassium (sometimes potassium secretion), and a return of excretion of calcium to control levels. These studies indicate that the parathyroid role in calcium and phosphate homeostasis in starlings is predominantly on the kidney.

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Angiotensin II and renal excretion of sodium and potassium in unanaesthetized dogs

Scandinavian Journal of Clinical and Laboratory Investigation ◽

10.3109/00365518209168055 ◽

1982 ◽

Vol 42 (1) ◽

pp. 87-92 ◽

Cited By ~ 5

Author(s):

H. C. Børresen ◽

S. Rørvik ◽

I. Guldvog ◽

A. Aakvaag

Keyword(s):

Angiotensin Ii ◽

Renal Excretion ◽

Sodium And Potassium

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CONGENITAL PITRESSIN RESISTANT DIABETES INSIPIDUS OF RENAL ORIGIN

PEDIATRICS ◽

10.1542/peds.15.3.298 ◽

1955 ◽

Vol 15 (3) ◽

pp. 298-372

Author(s):

William B. Macdonald

Keyword(s):

Diabetes Insipidus ◽

Extracellular Fluid ◽

Male Infant ◽

Renal Tubules ◽

Post Mortem ◽

Water Metabolism ◽

History Of ◽

Renal Clearances ◽

Renal Function Tests ◽

Renal Origin

1) The history of a male infant who presented soon after birth with features of failure to gain weight, dehydration and pyrexia of obscure origin, has been described. A diagnosis of pitressin resistant diabetes insipidus was made. 2) Renal function tests and post-mortem examination, including microdissection of the kidney, indicates that the basic defect in water metabolism was a functional inability of the distal renal tubules to respond to antidiuretic hormone. 3) Consequent dehydration was insufficient to cause circulatory collapse, but affected renal clearances. 4) There was evidence of increased catabolism and poor protein utilisation. 5) Hyperosmolarity of the extracellular fluid was accompanied by a rise in body temperature, probably due to a depression of sweat gland activity. 6) Post-mortem evidence suggests that infants with pitressin resistant diabetes insipidus should be investigated for cystine storage disease.

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Impact of hydrogen ion on fasting ketogenesis: feedback regulation of acid production

AJP Renal Physiology ◽

10.1152/ajprenal.1982.242.3.f238 ◽

1982 ◽

Vol 242 (3) ◽

pp. F238-F245 ◽

Cited By ~ 2

Author(s):

V. L. Hood ◽

E. Danforth ◽

E. S. Horton ◽

R. L. Tannen

Keyword(s):

Acid Production ◽

Metabolic Regulation ◽

Feedback Regulation ◽

Hydrogen Ion ◽

Acid Excretion ◽

Acid Base Balance ◽

Acid Base ◽

Urine Ph ◽

Ion Production ◽

Base Balance

To determine whether acid-base balance regulates hydrogen ion production, seven obese volunteers were given NaHCO3 and NH4Cl (2 mmol.kg-1.day-1) during two separate 7-day fasts. On days 5-7 plasma bicarbonate was lower in the NH4Cl fasts (14.0 +/- 1.4 mM) than in the NaHCO3 fasts (18.3 +/- 1.1 mM), while urine pH and net acid excretion did not differ. Acid production (acid excretion minus intake) was greater by 204 mmol/day in the NaHCO3 fasts (274 +/- 16 mmol/day) than in the NH4Cl fasts (70 +/- 19 mmol/day). Ketoacid excretion, which reflected net ketoacid production, paralleled acid production, decreasing from 213 +/- 24 mmol/day in the NaHCO3 fasts to 67 +/- 18 mmol/day in the NH4Cl fasts. Thus, during starvation, alterations in hydrogen ion intake and the associated changes in acid-base balance modify the net production of endogenous acid by influencing the synthesis or utilization of ketoacids. Although the specific site of this metabolic regulation is undefined, these results indicate that systemic acid-base status can exert feedback control over hydrogen ion production.

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Role of organic anions in renal response to dietary acid and base loads

AJP Renal Physiology ◽

10.1152/ajprenal.1989.257.2.f170 ◽

1989 ◽

Vol 257 (2) ◽

pp. F170-F176 ◽

Cited By ~ 11

Author(s):

J. C. Brown ◽

R. K. Packer ◽

M. A. Knepper

Keyword(s):

Organic Anion ◽

Organic Anions ◽

Acid Excretion ◽

Acid Base Balance ◽

Acid Base ◽

Urine Ph ◽

Renal Response ◽

Base Balance ◽

Net Acid Excretion

Bicarbonate is formed when organic anions are oxidized systemically. Therefore, changes in organic anion excretion can affect systemic acid-base balance. To assess the role of organic anions in urinary acid-base excretion, we measured urinary excretion in control rats, NaHCO3-loaded rats, and NH4Cl-loaded rats. Total organic anions were measured by the titration method of Van Slyke. As expected, NaHCO3 loading increased urine pH and decreased net acid excretion (NH4+ + titratable acid - HCO3-), whereas NH4Cl loading had the opposite effect. Organic anion excretion was increased in response to NaHCO3 loading and decreased in response to NH4Cl loading. We quantified the overall effect of organic ion plus inorganic buffer ion excretion on acid-base balance. The amounts of organic anions excreted by all animals in this study were greater than the amounts of NH4+, HCO3-, or titratable acidity excreted. In addition, in response to acid and alkali loading, changes in urinary organic anion excretion were 40-50% as large as changes in net acid excretion. We conclude that, in rats, regulation of organic anion excretion can contribute importantly to the overall renal response to acid-base disturbances.

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