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

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.

Meclofenamate and urine concentration with and without exposure of the renal papilla

1981 ◽  
Vol 240 (5) ◽  
pp. F423-F429 ◽  
Author(s):  
R. J. Roman ◽  
C. Lechene
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renal Papilla ◽  
Arterial Blood ◽  
Pelvic Urine

The recent finding that inhibitors of prostaglandin synthesis prevent the fall in urine concentration produced by papillary exposure challenges the hypothesis that contact between the pelvic urine and papilla is essential to the renal concentrating process. The present study examines the change in urine osmolality produced by exposure of the renal papilla in rats given meclofenamate. In control animals urine osmolality(Uosmol) decreased 57% after 2 h of exposure of the renal papilla. In rats given meclofenamate 4 mg/kg urine osmolality increased 16%, urine flow decreased 30%, and glomerular filtration rate was unchanged in the nonexposed kidney. Meclofenamate, however, did not alter the decrease in Uosmol seen in the kidney with the exposed papilla. Meclofenamate 10 mg/kg was also ineffective in preventing the fall in urine osmolality produced by papillary exposure, although this higher dose decreased glomerular filtration rate and arterial blood pressure. These results are consistent with the finding that pelvic urine urea is important to the urinary concentrating process and with the hypothesis that urine osmolality falls after papillary exposure because contact between pelvic urine and papilla is interrupted.

Angiotensin-(1–7) in the ovine fetus

2001 ◽  
Vol 280 (2) ◽  
pp. R404-R409 ◽  
Author(s):  
Karen M. Moritz ◽  
Duncan J. Campbell ◽  
E. Marelyn Wintour
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Filtration Rate ◽  
Plasma Concentrations ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Ang Ii ◽  
Arterial Blood

In the adult animal, ANG-(1–7) may counterbalance some effects of ANG II. Its effects in the fetus are unknown. Basal ANG-(1–7), ANG I, ANG II, and renin concentrations were measured in plasma from ovine fetuses and their mothers ( n = 10) at 111 days of gestation. In the fetus, concentrations of ANG I, ANG-(1–7), and ANG II were 86 ± 21, 13 ± 2, and 14 ± 2 fmol/ml, respectively. In the ewe, concentrations of ANG I were significantly lower (20 ± 4 fmol/ml, P < 0.05) as were concentrations of ANG-(1–7) (2.9 ± 0.6 fmol/ml), whereas ANG II concentrations were not different (10 ± 1 fmol/ml). Plasma renin concentrations were higher in the fetus (4.8 ± 1.1 pmol ANG I · ml−1 · h−1) than in the ewe (0.9 ± 0.2 pmol · ml−1 · h−1, P < 0.05). Infusion of ANG-(1–7) (∼9 μg/h) for a 3-day period caused a significant increase in plasma concentrations of ANG-(1–7) reaching a maximum of 448 ± 146 fmol/ml on day 3 of infusion. Plasma levels of ANG I and II as well as renin were unchanged by the infusion. Urine flow rate, glomerular filtration rate, and fetal arterial blood pressure did not change and were not different than values in fetuses receiving a saline infusion for 3 days ( n = 5). However, the osmolality of amniotic and allantoic fluid was significantly higher in fetuses that received ANG-(1–7). Also, compared with the saline-infused animals, mRNA expression levels of renin, the AT1 receptor, and AT2 receptor were elevated in kidneys of fetuses that received infusions of ANG-(1–7). Infusion of an ANG-(1–7) antagonist {[d-Ala7]-ANG-(1–7), 20 μg/h} for 3 days had no effect on fetal blood pressure or renal function. In conclusion, although infusion of ANG-(1–7) did not affect fetal urine flow rate, glomerular filtration rate, or blood pressure, changes in fetal fluids and gene expression indicate that ANG-(1–7) may play a role in the fetal kidney.

Effect of Citrate Infusion on Urinary Aluminium Excretion in the Rat

1994 ◽  
Vol 86 (2) ◽  
pp. 223-226 ◽  
Author(s):  
Malcolm Cochran ◽  
Vira Chawtur ◽  
John W. Phillips ◽  
Beverley Dilena
Keyword(s):  
Glomerular Filtration Rate ◽  
Plasma Level ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Urine Flow ◽  
Distilled Water ◽  
Aluminium Level ◽  
Excretion Rates ◽  
Urinary Citrate

1. Seven pairs of rats received 1 mmol/l aluminium citrate in their drinking water 5 days before the experiments. Five additional rats were treated identically. Six rats received the same food but drank distilled water. 2. After a 6 h fast, the animal was anaesthetized, the jugular vein and femoral artery were cannulated and the bladder was catheterized, after which an intravenous infusion of Hartmann's solution containing [14C]inulin was begun. The urine was collected at 20 min intervals and 1 ml of arterial blood was obtained before the end of each collection. After at least two basal collections, the infusion was modified to contain, in addition, 5 mmol/l NaHCO3 (control) or 5 mmol/l sodium citrate (experimental). The infusion rate, constant in each pair, differed between pairs across the range 60–125 μmol/min. 3. A total of eight collections was made per animal and urine flow, glomerular filtration rate, plasma and urinary aluminium and citrate were measured. 4. Control and experimental rats had a higher mean basal plasma aluminium level (0.39 ± 0.21 μmol/l) than the six rats receiving distilled water (0.16 ± 0.14 mmol/l, P < 0.001). The corresponding urinary aluminium excretion rates were similar (46 ± 31 and 47 ± 23 pmol/min, respectively). There was no significant difference between the basal values of any variable in the control and experimental rats. No significant change was observed in any variable during the infusion of NaHCO3 (controls). Among the experimental rats, there was no significant change in urine flow, glomerular filtration rate or plasma aluminium level. However, the plasma citrate level rose rapidly with the infusion to approach a plateau value in each case, and there were slower rises in urinary citrate and aluminium excretion rates. A renal threshold for citrate appeared to occur at a plasma level of approximately 0.25 mmol/l. The aluminium excretion rate was directly related to the citrate excretion rate (P < 0.01) and the increase in urinary aluminium excretion rate above the basal state was even more closely related (P < 0.001). 5. In the five additional animals pretreated with aluminium, the median ultrafiltrable aluminium was 20% (range 17–24%) of the total plasma level and no change was produced by citrate infused at the maximal rate. The plasma protein concentration also remained unchanged despite the fluid load. 6. We conclude that increased urinary citrate excretion is directly associated with an increase in aluminium excretion in aluminium-loaded animals. The data suggest that this increased excretion is independent of filtered load of aluminium and may therefore be the result of changes in handling of the metal within the kidney.

The Role of Prostaglandins in Glucagon-Induced Natriuresis

1980 ◽  
Vol 58 (5) ◽  
pp. 393-401 ◽  
Author(s):  
M. A. Kirschenbaum ◽  
E. T. Zawada
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin E ◽  
Excretion Rates

1. Three groups of anaesthetized dogs were studied to determine the role of renal prostaglandins in glucagon-induced natriuresis. 2. Urine flow, sodium and prostaglandin E excretion rates increased significantly in the experimental kidney with glucagon infusion (0.20 μg/min) into the renal artery. These changes were completely reversed after the administration of either of two inhibitors of prostaglandin synthesis. 3. Infusion of glucagon (0.20 μg/min) after the administration of either of the prostaglandin synthetase inhibitors failed to increase either urine flow rate or sodium excretion above control values and failed to elevate urine prostaglandin E excretion rates. 4. Infusion of glucagon (0.75–1.25 μg/min) resulted in significant elevations in urine flow rate, glomerular filtration rate, renal plasma flow, urine sodium and prostaglandin E excretion rates. 5. The data presented indicate that the diuresis and natriuresis seen with the infusion of glucagon (0.20 μg/min) are accompanied by an increase in urine prostaglandin E excretion and are reversed by the administration of inhibitors of prostaglandin synthesis, suggesting that the increased urine flow and sodium excretion rates are dependent on prostaglandin-mediated mechanisms. The administration of glucagon in higher doses appears to be associated with alterations in electrolyte excretion and glomerular filtration rate, which presumably is related to factors other than prostaglandin synthesis and release.

Amiloride-sensitive lithium reabsorption during doxazosin-induced blood pressure reduction in rats

1991 ◽  
Vol 81 (6) ◽  
pp. 809-814 ◽  
Author(s):  
Jørgen Søberg Petersen ◽  
Michael Shalmi ◽  
Martin Bak ◽  
Niels Lomholt ◽  
Sten Christensen
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Urine Flow ◽  
Lithium Clearance ◽  
Arterial Blood

1. The effects of acute systemic α1-anoceptor blockade by doxazosin on glomerular filtration rate, urine flow, sodium clearance and lithium clearance were investigated in acutely prepared conscious rats. 2. Clearance experiments were performed during water diuresis (20 mmol/l NaCl and 110 mmol/l glucose, 3 ml/h). After a control period, animals were randomized to one of the following treatments: time-control (n = 9), doxazosin (50 μg primer; 30 μg h−1 kg−1) (n = 10), amiloride (1 mg primer; 2.4 mg h−1 kg−1) (n = 10) and doxazosin plus amiloride (n = 9). 3. Doxazosin reduced the mean arterial blood pressure from 125 to 108 mmHg; this was associated with transient reductions in glomerular filtration rate, urine flow and lithium clearance. After the transient anti-diuresis, the sodium excretion rate remained reduced in doxazosin-infused animals. Amiloride increased the sodium excretion rate without having effects on other variables. When doxazosin was given together with amiloride, the reduction in lithium clearance observed during the transient reduction in glomerular filtration rate and urine flow, was partly abolished. Thus the fractional lithium excretion was transiently increased in rats given doxazosin plus amiloride (from 29 to 40%), whereas in rats given doxazosin alone a non-significant reduction was observed (from 28 to 25%). The dissociation between lithium clearance and fractional lithium excretion in the two doxazosin-infused groups was only significant during the transient reduction in glomerular filtration rate and urine flow. 4. The results provide evidence for an amiloride-sensitive lithium reabsorption during acute systemic α1-adrenoceptor blockade. It is suggested that activation of baroreflexes during the acute reduction in mean arterial blood pressure is responsible for stimulation of distal lithium reabsorption by an unknown mechanism.

DIAGNOSIS AND TREATMENT: ACUTE RENAL FAILURE

PEDIATRICS ◽  
1965 ◽  
Vol 35 (3) ◽  
pp. 478-481
Author(s):  
Malcolm A. Holliday
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Renal Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Obstructive Uropathy ◽  
Urine Flow ◽  
Water Restriction ◽  
Plasma Electrolyte

ACUTE RENAL FAILURE is an uncommon emergency which faces pediatricians. It is usually easy to recognize. The management in the early phase is critical to the survival potential of the patient. The purpose of this review is to cite the causes, characteristics, and principally the management of acute renal failure. Renal failure is defined as a state in which there is not sufficient kidney function to prevent the development of severe uremia or to maintain plasma electrolyte values in a range compatible with ordinary activities. Clinically the condition is associated with mental confusion, stupor, and frequently convulsions. Persistent hiccoughs, irregular respirations, and muscle cramps also may occur. Usually though not always, there is obvious oliguria. Since urine flow is ordinarily but 0.2-2,0% of glomerular filtration rate, and since glomerular filtration rate reduction to 5-10% may be associated with uremia, it is possible to have renal failure without oliguria. It is also possible to have physiological oliguria (&lt; 300 ml per square meter) in response to rigid water restriction that is not related to renal failure. Hence, the term must be defined in terms of its effect on plasma composition rather than in terms of urine flow. The presence of certain clinical conditions known to result in acute renal failure should alert the physician. These include: nephrotoxie agents; hemoglobinuria or myoglobinuria; shock with anoxic damage; acute, diffuse renal disease; acute dehydration in patients with chronic advanced renal disease; and acute obstructive uropathy. Nephrotoxic agents, hemoglobinuria, and shock all result in acute tubular necrosis, and recovery depends upon the capacity of the nephron to regenerate on an intact basement membrane.

Increased tubuloglomerular feedback activity in Milan hypertensive rats

1986 ◽  
Vol 250 (6) ◽  
pp. F967-F974 ◽  
Author(s):  
U. Boberg ◽  
A. E. Persson
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Single Nephron ◽  
Flow Pressure ◽  
Normotensive Strain

Studies of whole-kidney function and micropuncture measurements in superficial nephrons were performed to investigate the role of the tubuloglomerular feedback (TGF) in the excretion of salt and water in hydropenic and volume-expanded rats of the spontaneously hypertensive Milan strain (MHS). The rats were 3.5-5 and 5-7 wk old, and age-matched animals from the Milan normotensive strain (MNS) served as controls. There was no difference in mean arterial blood pressure (Pa) between the 3.5- to 5-wk-old prehypertensive MHS (MHSp) and MNS rats, but the glomerular filtration rate (GFR) was higher in MHSp than in MNS [1.35 vs. 0.80 ml X min-1 X g kidney wt (KW)-1, P less than 0.01]. The distal single-nephron glomerular filtration rate (SNGFR) was also higher in MHSp than in MNS (28.6 vs. 20.2 nl X min-1 X g KW-1, P less than 0.05). TGF was determined from both stop-flow pressure response and proximal and distal SNGFR. It was found that MHSp exhibited essentially no TGF response. During development of hypertension 5- to 7-wk-old MHS (MHSd) had a higher Pa than MNS (120 vs. 98 mmHg, P less than 0.01). Normally GFR and SNGFR increase with age, and such was the case with MNS (0.8 to 1.02 ml X min-1 X g KW-1 and 20.2 to 23.4 nl X min-1 X g KW-1), but in MHSd there was a decrease in both GFR and SNGFR with age (1.35 to 1.10 ml X min-1 X g KW-1 and 28.3 to 18.3 nl X min-1 X g KW-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal and hemodynamic effects of losartan in conscious dogs during controlled mechanical ventilation

1999 ◽  
Vol 276 (3) ◽  
pp. F425-F432 ◽  
Author(s):  
Martin O. Krebs ◽  
Thorsten Kröhn ◽  
Willehad Boemke ◽  
Rainer Mohnhaupt ◽  
Gabriele Kaczmarczyk
Keyword(s):  
Mechanical Ventilation ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Volume ◽  
Conscious Dogs ◽  
Positive End Expiratory Pressure ◽  
Arterial Blood ◽  
Controlled Mechanical Ventilation

In 12 conscious dogs, we investigated whether the angiotensin II-receptor antagonist losartan increases renal sodium excretion and urine volume during controlled mechanical ventilation (CMV) with positive end-expiratory pressure. In four experimental protocols, the dogs were extracellular volume (ECV) expanded (electrolyte solution, 0.5 ml ⋅ kg−1 ⋅ min−1iv) or not and received losartan (100 μg ⋅ kg−1 ⋅ min−1iv) or not. They breathed spontaneously during the 1st and 4th hour and received CMV with positive end-expiratory pressure (mean airway pressure 20 cmH2O) during the 2nd and 3rd hours. In the expansion group, dogs with losartan excreted ∼18% more sodium (69 ± 7 vs. 38 ± 5 μmol ⋅ min−1 ⋅ kg−1) and 15% more urine during the 2 h of CMV because of a higher glomerular filtration rate (5.3 ± 0.3 vs. 4.5 ± 0.2 ml ⋅ min−1 ⋅ kg−1) and the tubular effects of losartan. In the group without expansion, sodium excretion (2.0 ± 0.6 vs. 2.6 ± 1.0 μmol ⋅ min−1 ⋅ kg−1) and glomerular filtration rate (3.8 ± 0.3 vs. 3.8 ± 0.4 ml ⋅ min−1 ⋅ kg−1) did not change, and urine volume decreased similarly in both groups during CMV. Plasma vasopressin and aldosterone increased in both groups, and plasma renin activity increased from 4.9 ± 0.7 to 7.8 ± 1.3 ng ANG I ⋅ ml−1 ⋅ h−1during CMV in nonexpanded dogs without losartan. Mean arterial pressure decreased by 10 mmHg in nonexpanded dogs with losartan. In conclusion, losartan increases sodium excretion and urine volume during CMV if the ECV is expanded. If the ECV is not expanded, a decrease in mean arterial blood pressure and/or an increase in aldosterone and vasopressin during CMV attenuates the renal effects of losartan.

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