Further Studies on Segmental Sodium Transport in the Rat Kidney during Expansion of the Extracellular Fluid Volume

Osgood, Richard W.; Reineck, H. J.; Stein, Janice Gross

doi:10.1172/jci109131

Cited by 50 publications

(25 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Earley and Friedler (3) suggested that renal vasodilatation may cause a natriuresis as a consequence of the washout of the hypertonic medullary interstitium occurring in this setting. Furthermore, recent studies from this laboratory have suggested that medullary washout may preferentially depress sodium reabsorption in the more inner cortical nephrons (4).…”

Section: Introductionmentioning

confidence: 99%

Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Fadem¹,

Hernandez-Llamas²,

Patak³

et al. 1982

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

A B S T R A C T The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Yet the mechanisms involved in this natriuretic effect are not clear. Recent studies with another renal vasodilator, secretin have shown this drug also causes a profound increase in renal blood flow but without major changes in sodium excretion. To attempt to delineate the basis of this difference in sodium excretion with these drugs, the renal functional effects of secretin and bradykinin were compared at an equivalent vasodilating dose. Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115,ueq/min. Urine osmolality fell from 1,230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, sodium excretion, and urine osmolality were significantly less.In further studies papillary plasma flow was estimated using the albumin accumulation technique. Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 seq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Studies with acetylcholine were qualitatively similar to those of bradykinin. Renal blood flow increased from 150 to 248 ml/min, urinary sodium excretion increased from 20 to 243 geq/min, urinary osmolality decreased from 1,237 to 411 mos-

show abstract

Section: Introductionmentioning

confidence: 99%

Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Fadem¹,

Hernandez-Llamas²,

Patak³

et al. 1982

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

show abstract

“…In contrast, the FeNa of the superficial nephrons is affected by either procedure. In addition, these authors have demonstrated that after expansion with Ringer's solution the natriuretic response of the superficial nephrons is smaller than that of the nephrons located deep in the cortex (18,19). The results of our previous studies in young animals sustaining saline expansion (7) suggested to us that the observations of Osgood et al might be relevant to our understanding of the development of the natriuretic response to volume expansion.…”

Section: Discussionmentioning

confidence: 78%

“…Experiments performed by Osgood et al (18,19) have provided evidence that the expansion with Ringer's solution suppresses FeNa in the juxtamedullary nephrons,-whereas expansion with hyperoncotic albumin fails to do so. In contrast, the FeNa of the superficial nephrons is affected by either procedure.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Intravascular Volume Expansion and Natriuresis in Developing Puppies

1982

View full text Add to dashboard Cite

SummaryThe role played by the relative degree of expansion of the intravascular and extravascular compartments in limiting the natriuretic response of fluid-loaded developing animals was determined in I-, 2-, 3-and 6-wk-old puppies. Volume expansion was induced by infusing either isotonic saline, 10% body weight or isoncotic albumin in saline 5% body weight, and measurements of giomerular filtration rate, sodium excretion, fractional excretion of sodium, and plasma volume were made. Each expansion procedure resulted in an increase in the absolute excretion of sodium at all ages ( P < 0.001). The greatest natriuretic effect was observed in the 3-wk-old puppies, the average of the two solutions being 19, 30, 70, and 28 pEq/min/kg in the 1, 2, 3, and dwk-old animals, respectively. The difference in natriuresis among the age groups was due predominantly to differences in the magnitude of the increase fractional excretion of sodium. At all ages, a greater absolute excretion of sodium was encountered during volume expansion with saline than observed with albumin ( P < 605). The intravascular volume increased by a similar % at all ages (P > 0.1), and saline and albumin yielded equivalent degrees of intravascular expansion (approximately 50%). The results demonstrate that age-related changes in natriuretic response to volume expansion cannot be attributed to differences in either the degree of expansion or the distribution of the load. In addition, the observations indicate that the mechanism underlying the difference between the response to isotonic saline and isoncotic albumin in saline is already operative at birth, and that it is independent of nephron heterogeneity since the proportion of superficial nephrons must have changed during the period of nephrogenesis. SpeculationThe collecting duct, which is sensitive to both isotonic saline and isoncotic albumin, is likely to be responsible for the parallel development of the renal response to these two methods of intravascular volume expansion.It has been amply demonstrated that the excretory response to saline expansion is less in neonatal and developing animals than it is in mature subjects (1,7,12,13,16). Early investigators have suggested that the low glomerular filtration rate (GFR), which prevails during this period of development, limits the natriuresis elicited by volume expansion. This concept has been recently challenged. Our work (7) and that performed by others (12,13) have demonstrated that an avid reabsorption by the renal tubule rather than a low GFR is the main cause of the limited natriuresis observed in infancy. The mechanism responsible for the persistence of a high fractional reabsorption in developing animals, even under conditions of volume expansion, has not as yet been established. We reasoned that "immaturity" of the transport mechanism could not provide an adequate explanation for this phenomenon because reabsorption of sodium is a process that requires the expenditure of energy, and as such it might be expected to be less efficient in the dev...

show abstract

“…Our studies (8) and those of others (9) have indicated that 10% body weight Ringer loading preferentially inhibits sodium reabsorption in juxtamedullary nephrons. More recently, we (10) suggested that this phenomenon was at least partially due to washout of the hypertonic medullary interstitium. Nevertheless, direct support for an important role of medullary tonicity in the control of urinary sodium excretion has been lacking.…”

Section: Introductionmentioning

confidence: 93%

Effect of Medullary Tonicity on Urinary Sodium Excretion in the Rat

Reineck¹,

Parma²

1982

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

A B S T R A C T In previous reports from this laboratory we have suggested that a reduction in medullary tonicity decreases the thin ascending loop of Henle sodium reabsorption and is in part responsible for the magnitude for the natriuresis accompanying 10% body weight Ringer loading. According to this postulate, one would expect that the medullary washout associated with water diuresis would also result in a natriuresis, but this does not occur. It is possible, however, that increased delivery from the proximal tubule is necessary to demonstrate an effect of medullary tonicity on urinary sodium excretion. Micropuncture studies were designed to test that possibility by increasing distal delivery by 2% Ringer loading in animals with and without reduced medullary tonicity. In an initial series of experiments the a-adrenergic agonist clonidine was used to induce a water diuresis. When given alone, this agent caused a marked decrease in urine osmolality and an increase in urine flow rate but had no effect on proximal reabsorption in either superficial or juxtamedullary nephrons, and did not alter urinary sodium excretion. Volume expansion with 2% body weight Ringer solution resulted in a significant fall in proximal reabsorption and a trivial increment in sodium excretion. When this same degree of volume expansion was conferred on animals undergoing a water diuresis, a marked increase in absolute and fractional sodium excretion occurred. In a second group of studies medullary tonicity was reduced in the left kidney only by removal of the left ureter 1 h before micropuncture. When these animals were infused with 2% body weight Ringer solution, proximal reabsorption was decreased in juxtamedullary nephrons, and a marked increase in sodium excretion was observed only from the left kidney. Finally, the effect of water diuresis on fractional sodium delivery to the early and late distal tubule of superficial nephrons during 2% Ringer loading was evaluated. Delivery to both of these sites was comparable after 2% Ringer loading alone and during 2% Ringer loading plus water diuresis.From these data, we conclude that medullary tonicity does influence renal sodium handling but that this effect is manifest in the final urine only under conditions in which proximal reabsorption is decreased. The data also suggest that this effect is limited to juxtamedullary nephrons and is probably localized to the thin ascending limb of the loop of Henle.

show abstract

Further Studies on Segmental Sodium Transport in the Rat Kidney during Expansion of the Extracellular Fluid Volume

Cited by 50 publications

References 31 publications

Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

The Relationship between Intravascular Volume Expansion and Natriuresis in Developing Puppies

Effect of Medullary Tonicity on Urinary Sodium Excretion in the Rat

Contact Info

Product

Resources

About