Non-linear partitioning and organic volatility distributions of urban aerosols.

Gas-to-particle partitioning of organic aerosols (OA) is represented in most models by Raoult's law, and depends on the existing mass of particles into which organic gases can dissolve. This raises the possibility of non-linear response of particle-phase OA mass to the emissions of precursor volatile organic compounds (VOCs) that contribute to this partitioning mass. Implications for air quality management are evident: a strong non-linear dependence would suggest that reductions in VOC emission would have a more-than-proportionate benefit in lowering ambient OA concentrations. Chamber measurements on simple VOC mixtures generally confirm the non-linear scaling between OA and VOCs, usually stated as a mass-dependence of the measured OA yields. However, for realistic ambient conditions including urban settings, no single component dominates the composition of the organic particles, and deviations from linearity are presumed to be small. Here we re-examine the linearity question using volatility spectra from several sources: (1) chamber studies of selected aerosols, (2) volatility inferred for aerosols sampled in two megacities, Mexico City and Paris, and (3) an explicit chemistry model (GECKO-A). These few available volatility distributions suggest that urban OA may be only slightly super-linear, with most values of the normalized sensitivity exponent in the range 1.1-1.3, also substantially lower than seen in chambers for some specific aerosols. The rather low exponents suggest that OA concentrations in megacities are not an inevitable convergence of non-linear effects, but can be addressed (much like in smaller urban areas) by proportionate reductions in emissions.

Phases of fluid and electrolyte homeostasis in the extremely low birth weight infant.

OBJECTIVE: We had shown previously that preterm infants undergo three phases of fluid and electrolyte homeostasis; prediuretic, diuretic, and postdiuretic. The objectives of the present study were: (1) to determine whether infants even more immature and infants cared for under thermal environmental conditions different from those previously studied also undergo these three phases; and (2) to relate these phases to changes in renal function. METHODS: Consecutive, timed urine collections were made during the first 5 days of life in 32 infants with birth weights of 1000 g or less. Infants were cared for in radiant warmers for 24 hours and then transferred to nonhumidified incubators. Diuresis was defined as urine flow rate (V) of 3 mL or more/kg per hour and weight loss of 0.8 g or more/kg per hour. The physiologic relationships among water and sodium balance, insensible water loss, arterial blood pressure, and renal function were made during the three phases. RESULTS: Twenty-eight (87%) of the 32 infants underwent the three homeostatic phases. The median ages of onset and cessation of diuresis were 25 and 96 hours, respectively. There was no correlation between onset of diuresis and change of thermal environment. During the prediuretic phase, V averaged 1.6 mL/kg per hour, and 17 of 28 infants had at least one collection period in which V was less than 1 mL/kg per hour; urinary sodium excretion was 0.1 mEq/kg per hour; the glomerular filtration rate (GFR) was 0.22 mL/kg per hour; fractional excretion of sodium (FENa) was 6.2%; and urine osmolality was dilute (221 mOsm/kg). During the diuretic phase, V and sodium excretion more than tripled; GFR and FENa doubled; and there was no change in urine osmolality. During postdiuresis, V and Na excretion decreased to values intermediate between the prediuretic and diuretic phases, and FENa fell to prediuretic levels, but there was no change in GFR or urine osmolality. There was poor correlation between blood pressure and GFR. Insensible water loss was high and variable during all phases, exceeding 190 mL/kg per day in the smallest infants. CONCLUSIONS: Extremely low birth weight infants manifest three phases of fluid and electrolyte homeostasis, as do more mature infants, independent of thermal environment. Diuresis and natriuresis are the result of abrupt increases in GFR and FENa. We speculate that this may be the result of expansion of the neonatal extracellular space as fetal lung fluid is reabsorbed.

Renal function correlates of postnatal diuresis in preterm infants.

A characteristic pattern of fluid homeostasis occurs in the first week of life in many preterm infants. Initially, urine output is low independent of fluid intake, subsequently a diuresis occurs, and finally urine output begins to vary with intake. Renal clearance measurements were made during each of these three phases to elucidate the renal mechanisms involved. Periods during which the ratio of urine output to fluid intake was greater than or equal to 1 and urine output was greater than or equal to 3 mL/kg/h were defined as diuretic. Of 22 preterm infants studied from 12 to 120 hours of age, 17 had at least one period of diuresis. In these infants, urine output, fluid intake rate, output to intake ratio, glomerular filtration rate, and fractional sodium excretion were lowest at 12 to 24 hours of age. During diuresis, urine output tripled without a significant change in fluid intake so that output to intake increased to levels exceeding unity. Diuresis was associated with significant increases in glomerular filtration rate and fractional sodium excretion. By 108 to 120 hours of age, urine output decreased despite an increase in fluid intake. This was accompanied by a decrease in glomerular filtration rate. These results suggest that the initial antidiuretic phase is the result of a low fractional sodium excretion in the face of a low glomerular filtration rate. Subsequently, diuresis and natriuresis occur as a result of abrupt, nonmaturational increases in glomerular filtration rate and fractional sodium excretion. With cessation of diuresis, glomerular filtration rate and fractional sodium excretion decrease and water and electrolyte output begin to vary appropriately with intake.

Renal bicarbonate excretion in extremely low birth weight infants.

OBJECTIVE: To test the hypothesis that due to the immaturity of their kidneys extremely low birth weight infants lose large amounts of bicarbonate in their urine. METHODS: Urine and blood samples collected every 8 to 12 hours for the first 4 days of life from 22 preterm infants 23 to 29 weeks' gestation weighing 540 to 982 g at birth were prospectively studied. RESULTS: As described previously, three phases of fluid homeostasis were identified. The first phase (prediuresis) was a period of low urine output followed by a period of spontaneous diuresis/natriuresis (diuretic phase) and then by a phase when urine output varied according to fluid intake (postdiuresis). Sodium, potassium, chloride, and bicarbonate excretion rates and bicarbonate balance (bicarbonate or acetate infused minus bicarbonate excreted) were calculated for each of the three phases. Urinary excretion of sodium, potassium, chloride, and bicarbonate increased from the prediuretic to the diuretic phase and decreased from the diuretic to the postdiuretic phase. During the diuretic phase 88% of renal sodium excretion was accompanied by excretion of chloride. Bicarbonate balance was positive in all three fluid phases. Cumulative renal bicarbonate loss over the first 4 days of life was 1.9 +/- 0.5 meq/kg (SD) and the cumulative bicarbonate balance was +4.4 +/- 4.1 meq/kg (SD). The glomerular filtration rate, filtered load of bicarbonate, and absolute tubular reabsorption of bicarbonate significantly increased from the prediuretic to the diuretic phase, while fractional reabsorption of sodium and chloride decreased between these two phases. The fractional reabsorption of bicarbonate did not change from prediuresis to diuresis, but increased from diuresis to postdiuresis and consequently from prediuresis to postdiuresis. CONCLUSIONS: Contrary to our original hypothesis, the total renal bicarbonate excretion of extremely low birth weight infants in the first 4 days of life is low and the net bicarbonate balance is positive. The anion predominantly accompanying the excretion of sodium in all three phases is chloride and not bicarbonate. Bicarbonate excretion appears to be independent of sodium excretion during these phases. The increase in renal tubular bicarbonate reabsorption during the first week of life may be associated with extracellular volume contraction.

Preservation of cerebral autoregulation in the unanesthetized hypoxemic newborn dog.

Studies were conducted to determine the effects of hypoxemia on cerebral blood flow and the influence of hyperoxia and hypoxemia on autoregulation of cerebral blood flow in the unanesthetized newborn dog. Twenty-one newborn dogs less than 2 weeks of age were studied. Cerebral blood flow was measured using radioactive microspheres during successive periods of normotension, hypotension (produced by blood withdrawal) and normotension (produced by infusion of previously withdrawn blood). In the hyperoxic animals, arterial pO2 was maintained above 250 torr by having the animal breathe 100% oxygen, while in the hypoxemic animals arterial pO2 was maintained between 30 and 35 torr by having the animal breathe 12% O2. Cerebral blood flow increased significantly with hypoxemia. In both hypoxemic and hyperoxic animals cerebral blood flow was maintained constant in spite of a large fall in arterial blood pressure and cardiac output, demonstrating the presence of autoregulation. Calculated oxygen transport to the brain was constant during hypoxemia and hypotension in all animals. Thus autoregulation of cerebral blood flow is present in newborn animals and is preserved under conditions of moderate hypoxemia.

The effect of metabolic acidosis upon autoregulation of cerebral blood flow in newborn dogs.

The radioactive microsphere technique was used in 13 newborn dogs to determine the effect of a metabolic (lactic)acidosis upon cardiac output (CO), cerebral blood flow (CBF), and autoregulation of cerebral blood flow. The animals were mechanically ventilated with supplemental oxygen to ensure normocarbia and hyperoxia throughout the experiments. Baseline cardiac output and cerebral blood flow measurements were made, followed by a lactic acid infusion to maintain pH less than 7.25. Metabolic acidosis produced a 27% fall in cardiac output and no change in cerebral blood flow (19 ml/100 g/min). Autoregulation was tested in 6 of the acidemic puppies by acute volume depletion to reduce blood pressure by 30% of baseline, followed by rapid volume re-expansion of the withdrawn blood. With volume depletion, CO decreased by 38%, and with volume re-expansion CO returned to baseline. The CBF remained at baseline levels with volume depletion but was slightly increased after rapid volume re-expansion. Five acidemic controls maintained CO and CBF constant with time. Thus cerebral autoregulation is preserved in the newborn dogs during metabolic acidosis, although cerebral blood flow was slightly increased following volume re-expansion.

Effects of Carbicarb and sodium bicarbonate on hypoxic lactic acidosis in newborn pigs.

BACKGROUND: Use of sodium bicarbonate (NaHCO3) may result in intracellular acidosis due to the generation of CO2. Carbicarb, has been reported to be superior to sodium bicarbonate (NaHCO3) because of lesser generation of CO2. The present study was designed to investigate whether Carbicarb or NaHCO3 is superior to normal saline in the treatment of hypoxic lactic acidosis. METHODS: Hypoxia was induced by ventilation with 8% O(2) in 30 piglets with fixed ventilation. When the pH fell to < 7.2, hypoxia was reversed by placing the animals in 21% O2 (experiment 1) or 100% O(2) (experiment 2) and either saline, Carbicarb or NaHCO3 were given. Data were collected for 120 minutes after therapy. RESULTS: In both experiment 1 (severe acidosis, pH < or = 7.1) and 2 (moderate acidosis, pH < or = 7.2) use of Carbicarb and NaHCO3 increased the arterial carbon dioxide tension (pCO2) significantly (p < 0.05). With moderate acidosis: 1) use of alkalinizing agents compared to saline resulted in an initial improvement in arterial pH at 1 minute, but thereafter, the differences were not statistically significant; and 2) there were no differences in hemodynamic variables and plasma lactic acid concentration between the three groups. CONCLUSIONS: The data demonstrate that 1) both Carbicarb and NaHCO3 significantly increase arterial pCO2; and 2) use of either alkalinizing agent in moderate acidosis does not alter the course of acidosis.

Renal bicarbonate reabsorption in the new-born dog.

1. Renal bicarbonate reabsorption was measured in thirty new-born dogs 2-27 days of age. Plasma bicarbonate was varied in the puppies by exchanging their blood with blood containing high levels of bicarbonate and low levels of chloride.2. The exchange transfusion resulted in increases of plasma pH, P(CO2) and bicarbonate in the puppies without changing plasma sodium and potassium or glomerular filtration rate (g.f.r.) and body weight.3. There was no tubular reabsorption maximum (T(m)) for bicarbonate and reabsorption values as high as 50 muequiv/ml. g.f.r. could be attained. No animals excreted bicarbonate at plasma levels below 25 mM and some animals had plasma bicarbonate threshold values in excess of 40 mM.4. Bicarbonate reabsorption increased as arterial P(CO2) rose (r = 0.62) but this was due to the rise of filtered bicarbonate since (a) there was no correlation between arterial P(CO2) and bicarbonate reabsorption when factored by filtered bicarbonate and (b) lowering arterial P(CO2) by mechanical hyperventilation did not reduce bicarbonate reabsorption corrected for filtered load.5. Inhibition of renal carbonic anhydrase by acetazolamide (50 mg/kg) resulted in an inhibition of bicarbonate reabsorption of only 4.5 muequiv/ml. g.f.r. (less than 20% of the total). Even with renal carbonic anhydrase inhibited, there was no bicarbonate T(m) and bicarbonate reabsorption values as high as 40 muequiv/ml. g.f.r. could be attained.6. There was good correlation (r = 0.82) between inhibition of sodium and bicarbonate reabsorption during renal carbonic anhydrase inhibition. However, with carbonic anhydrase inhibited, there was no correlation between arterial P(CO2) and bicarbonate reabsorption.7. These results demonstrate that tubular bicarbonate reabsorption mechanisms in the new-born dog are as efficient as those reported for the adult as long as body fluid and plasma sodium and potassium levels are carefully maintained.8. The results are also consistent with a bicarbonate reabsorptive mechanism explained either by direct ionic bicarbonate reabsorption or by hydrogen ion secretion with diffusion of carbonic acid.

Renal sodium reabsorption during saline loading and distal blockade in newborn dogs.

The ability of the proximal tubule to respond to saline expansion and varying filtered sodium loads was studied in 27 neonatal dogs aged 1-23 days. Sodium reabsorption beyond the proximal tubule was blocked with ethacrynic acid and chlorothiazide. When puppies received an intravenous load of 0.9% saline for 1.5 h, fractional sodium reabsorption averaged 0.985. After the addition of distal blockade to the saline infusion fractional Na reabsorption fell to 0.512. During distal blockade alone fractional Na reabsorption was 0.701, and after 1.5 h of saline expansion added to distal blockade fractional Na reabsorption fell to 0.493. Thus, there was a significant decrease in proximal tubular fractional Na reabsorption after saline expansion in neonatal dogs, and the high fractional Na reabsorption and low Na excretion during saline loading without distal blockade must be due to a large distal Na reabsorption. When filtered sodium load was varied by raising and lowering the glomerular filtration rate during distal blockade, there was excellent correlation between amount of filtered and reabsorbed sodium (r = 0.92). Thus, glomerulotubular balance exists in newborn dogs when there is no saline expansion.

Renal osmotic effect of mannitol in the neonatal and adult dog.

The renal response to mannitol loading was studied in 21 newborn dogs aged 1-19 days and in 12 adult dogs. One group of animals (protocol B) underwent distal nephron blockade with ethacrynic acid and amiloride prior to and during infusion of mannitol to estimate proximal tubule function. The other group of animals (protocol A) received mannitol without the diuretics. Mannitol was infused at progressively increasing dosages, resulting in progressively increasing mannitol excretion rates. For all groups of animals, as mannitol excretion rates increased, urine flow and sodium, potassium, and chloride excretion rates increased. However, there was no correlation between mannitol excretion and bicarbonate excretion. The osmotic effect of mannitol was quantitated from the slope of the plot of mannitol excretion vs. sodium excretion (dNa/dMan). In both pups and adults dNa/dMan was greater in protocol B (1.47 for pups, 0.70 for adults) than in protocol A (0.18 for pups, 0.07 for adults). In addition, in protocol B dNa/dMan was greater in the newborn than in the adult and decreased logarithmically with age in pups. In protocol B, as mannitol excretion increased, the urine-to-plasma sodium ratio declined in adults but did not change in pups. Urine-to-plasma osmolality ratio remained at unity throughout the experiment in both age groups in protocol B. These results indicate that 1) the osmotic effect of mannitol is greater in the immature than in the mature kidney, and 2) the greater osmotic effect in the neonatal kidney is related to inability of the immature proximal tubule to generate and sustain a transtubular sodium gradient.

Pressure natriuresis during saline expansion in newborn and adult dogs.

Pressure natriuresis was studied in anesthetized saline-expanded adult (n = 10) and neonatal (n = 23) dogs. One group (protocol B) received ethacrynic acid and amiloride to block distal nephron function. Studies in the other group (protocol A) were done without diuretics. Renal arterial blood pressure was raised by bilateral carotid artery occlusion. Renal perfusion pressure was then lowered in steps by partially occluding the aorta proximal to the renal arteries. In protocol B carotid occlusion was associated with an increase in both absolute and fractional sodium excretion by adult and newborn dogs. Moreover, there was significant negative correlation (P less than 0.01) between absolute change in renal arterial pressure and change in tubular reabsorption of sodium per milliliter glomerular filtrate for both age groups. For each mmHg increase in blood pressure there was greater inhibition of sodium reabsorption in the puppy (0.55 mueq/ml glomerular filtrate) than in the adult (0.18 mueq/ml, P less than 0.05). In protocol A puppies, the inhibition of sodium reabsorption due to increases in renal perfusion pressure was less than that occurring in protocol B, indicating that some of the sodium escaping proximal nephron reabsorption was reabsorbed distally. Results of these studies indicate that during saline expansion pressure natriuresis is primarily a proximal tubular event, and the sensitivity of the proximal tubule to changes in renal arterial blood pressure is greater in the newborn than the adult kidney.

Segmental nephron sodium and potassium reabsorption in newborn and adult dogs during saline expansion.

Studies were carried out in 23 anesthetized neonatal dogs aged 2 to 20 days and in 16 adult dogs to compare the effects of saline volume expansion on renal tubular Na and K reabsorption between newborn and adult animals. Proximal- and distal-tubule function was estimated by the distal-nephron-blockade technique using ethacrynic acid and amiloride. During saline infusion, which increased extracellular volume by approximately 30% for both age groups, total nephron fractional Na reabsorption was 0.91 for the adult but 0.98 for the puppy (P less than 0.01). However, proximal tubule fractional Na reabsorption was greater in the adult (0.64) than in the puppy (0.48, P less than 0.01) whereas distal nephron fractional Na reabsorption was much greater in the newborn (0.51) than in the adult (0.26, P less than 0.01). Sodium reabsorption normalized to kidney weight was lower in all segments of the neonatal kidney than in the adult kidney. The filtered sodium load was lower in the newborn (27.0 mueq min-1g-1) than in the adult (105.0, P less than 0.01), and the Na load to the distal nephron was also lower in the newborn (14.0 mueq min-1g-1) than in the adult (37.2, P less than 0.01). Fractional K excretion was similar in both age groups even though the fraction of filtered K escaping proximal-tubule reabsorption was greater in the newborn than in the adult, indicating greater net K fractional reabsorption in the distal nephron of the newborn than in the adult kidney. These results indicate that in response to saline expansion there is a greater proximal tubule natriuresis in the neonate than in the adult but overall renal Na excretion is less in the newborn animal due to enhanced fractional Na reabsorption in the neonatal distal nephron, particularly in Henle's Loop. This increase in distal nephron fractional sodium reabsorption may be related in part to the relatively small absolute Na load presented to the distal nephron of the neonatal kidney.

Effects of euvolemic and hypervolemic hyperbicarbonemia on segmental nephron HCO3 reabsorption in the newborn dog.

Studies were undertaken to determine the effect of elevated plasma bicarbonate concentration (PHCO3) with and without volume expansion on segmental nephron HCO3 reabsorption in newborn and adult dogs using the technique of distal blockade. Reabsorption of bicarbonate per mL glomerular filtrate (RHCO3/GFR) in the proximal nephron was more suppressed in euvolemic newborns than euvolemic adults as PHCO3 was increased from baseline to 50-70 mM. Inasmuch as total nephron reabsorption has been shown to be essentially complete under these conditions in both newborns and adults, distal nephron HCO3 delivery and the fraction of the distal HCO3 load reabsorbed must have been greater in euvolemic newborns than adults when PHCO3 was elevated. Total nephron RHCO3/GFR was less suppressed by NaHCO3 volume expansion in the newborn than it was in the adult. However, proximal nephron RHCO3/GFR was similarly suppressed by NaHCO3 volume expansion in newborns and adults. Thus, the NaHCO3-expanded newborn must have reabsorbed a greater proportion of the increased distal HCO3 load than did the NaHCO3-expanded adult. Proximal nephron HCO3 reabsorption is a balance between reabsorption effected by active proton secretion and passive HCO3 back leak. Euvolemic increase in peritubular HCO3 concentration has been shown to suppress proximal tubular proton secretion; volume expansion increases proximal tubule HCO3 permeability and back leak.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acute polycythemia on newborn renal hemodynamics and function.

The present study investigates the effects of polycythemia on renal hemodynamics and function in 15 anesthetized newborn dogs, 2-10 days of age. Microspheres were used to study renal blood flow. Experimental animals received an exchange transfusion with adult dog packed red blood cells resulting in an increase in hematocrit from 38% +/- 2.1% to 69% +/- 2.1%. Control animals received an exchange transfusion with adult dog whole blood so that there was no change in hematocrit. Polycythemia resulted in a marked increase in blood viscosity, a 40% fall in cardiac output from 251.8 +/- 14 ml/kg/min to 150.7 +/- 9 ml/kg/min and a 98% increase in total vascular resistance from 0.32 +/- 0.02 mmHg/ml/kg/min to 0.63 +/- 0.07 mmHg/ml/kg/min. Nevertheless, renal blood flow was not significantly altered indicating renal vasodilation (1.4 +/- 0.06 ml/g/min initial versus 1.2 +/- 0.09 ml/g/min final). Although renal blood flow was well preserved, renal plasma flow decreased by 63% as the hematocrit increased from 0.86 +/- 0.03 ml/g/min to 0.38 +/- 0.04 ml/g/min, resulting in a 53% fall in glomerular filtration rate from 0.21 +/- 0.02 ml/min/g kidney weight to 0.09 +/- 0.02 ml/min/g kidney weight. There was also a large drop in urine output and Na and K excretion following polycythemia. This was due primarily to the decreased filtered load, because fractional Na reabsorption remained constant. Thus, in spite of well-preserved renal blood flow, polycythemia markedly affected renal function, resulting in water and salt retention.

Chloride concentration gradient in newborn dogs in the presence of distal nephron blockade.

Renal tubular Na+, Cl-, and H2O reabsorption was determined in 14 newborn dogs, 3--29 days of age, and in three adult dogs. In all animals NaCl reabsorption beyond the proximal tubule was blocked with ethacrynic acid (2 mg/kg) and amiloride (2.4 mg/kg). During distal blockade, fractional reabsorption of NaCl and water in both newborns and adults was approximately 70%, and there was a urine-to-plasma chloride gradient equal to 1.34 +/- 0.01, indicating that the proximal tubules of the newborn as well as those of the adult can generate a transtubular Cl- gradient. Upon administration of acetazolamide (50 mg/kg), there was a dramatic increase in excretion of Na+, Cl-, HCO3-, and water, and a decrease in the transtubular chloride gradient. After acetazolamide, the degree of inhibition of HCO3 reabsorption was well correlated with that of Na+, (r = 0.77) or Cl- (r = 0.74), and Na+ or Cl- inhibition exceeded that of HCO3-. In the newborn animal, the ratio of inner-to outer cortical nephron function is high at birth and declines rapidly during the first few weeks of life. However, there was no correlation between age and changes in either electrolyte excretion or in the transtubular chloride gradient. Therefore, the newborn dog possesses Cl- permselective tubules in the inner cortex that, in the presence of intact HCO3- reabsorption, are capable of establishing a functional transtubular Cl- gradient contributing to NaCl reabsorption.

Natriuretic effect of oxytocin on saline-expanded neonatal dogs.

The natriuretic effect of oxytocin was studied in 40 anesthetized newborn dogs 2-33 days of age. After saline expansion, puppies excreted only 2.86% of the filtered sodium (adult dogs undergoing similar volume expansion excrete about 65-8% of the filtered sodium). After oxytocin was infused in these saline-expanded puppies at 8 mU x kg-1 x h-1, fractional sodium excretion increased to 7.51%. Oxytocin had no natriuretic effect in nonexpanded puppies. In nonexpanded animals, when distal nephron function was blocked by a combination of ethacrynic acid, chlorothiazide, and amiloride, fractional sodium excretion averaged 31%. In contrast, distal nephron blockade in saline-expanded animals resulted in fractional sodium excretion of 55%. When oxytocin was infused in either saline-expanded or nonexpanded puppies undergoing distal nephron blockade, there was no increase in sodium excretion. These results support the following conclusions. In the newborn dog 1) the attenuated natriuretic response to saline expansion is related to increased reabsorption of sodium in the distal nephron; 2) an adult type of natriuretic response to saline expansion can be induced in puppies by infusion of oxytocin; and 3) oxytocin inhibits sodium reabsorption in the distal nephron.

Effect of amiloride on the renal response to saline expansion in new-born dogs.

1. The renal effects of amiloride were studied in twenty-six new-born and nine adult dogs, with and without saline expansion. 2. Without saline expansion, amiloride inhibited more sodium reabsorption (normalized to GFR) in puppies than in adults (5.95 vs. 2.18 muequiv/ml. GFR, P less than 0.01). Amiloride inhibited sodium reabsorption more in saline expanded than in nonexpanded puppies (9.39 vs. 5.95 muequiv/ml. GFR, P less than 0.01) but there was no difference between expanded and non-expanded adults. 3. Saline expansion by itself increased fractional sodium excretion (CNa/GFR) more in the adult than in the puppy (0.071 vs. 0.019, P less than 0.01). During amiloride inhibition, saline expansion increased CNa/GFR to 0.045 in the puppy (compared to 0.019 in the nonamiloride inhibited puppy) but saline expansion increased CNa/GFR to the same degree in the amiloride as in the non-amiloride inhibited adult. 4. In all puppies amiloride inhibited more sodium reabsorption than potassium secretion and there was poor correlation between the degree of inhibition of sodium reabsorption and potassium secretion for both the puppy (r = 0.14) and the adult (r = 0.05). 5. Assuming that amiloride acts by inhibiting sodium reabsorption and potassium secretion in the late distal and cortical collecting tubules, these results support the conclusion that in these regions of the nephron of the new-born dog (a) a greater fraction of the filtered sodium is reabsorbed than in the adult and (b) increased fractional sodium reabsorption is responsible, in part, for the attenuated natriuretic response to saline expansion.