Skip to main content
NCBI home page
The Journal of Clinical Investigation logoLink to The Journal of Clinical Investigation
. 1974 Dec;54(6):1428–1436. doi: 10.1172/JCI107890

Dependence of Saline-Induced Natriuresis upon Exposure of the Kidney to the Physical Effects of Extracellular Fluid Volume Expansion

John P Fitzgibbons 1,2, F John Gennari 1,2, Howard B Garfinkel 1,2, Stanley Cortell 1,2
PMCID: PMC301698  PMID: 4436441

Abstract

In many previous studies, the natriuresis induced by saline loading has been demonstrated to persist even though glomerular filtration rate (GFR) has been decreased to below pre-expansion levels by a reduction in renal artery pressure. In such studies, however, the kidney has been exposed to the effects of volume expansion for varying periods of time before renal artery pressure was controlled. The present experiments were designed to evaluate whether this period of exposure induces critical changes in intrarenal factors that are responsible for the natriuresis.

Experiments were carried out in rats, in which renal artery pressure was decreased to 70 mm Hg either at the onset of saline loading (immediate clamping experiments) or after 45 min of saline loading had elapsed (delayed clamping experiments). In the delayed clamping experiments, consonant with previous studies, mean sodium excretion, 3.2 μeq/min, remained markedly increased above control, despite a reduction in GFR to 91% of the hydropenic control value. In contrast, when renal artery pressure was comparably reduced at the onset of saline loading mean sodium excretion was only trivially increased, 0.4 μeq/min, although GFR increased to 140% of the hydropenic control value.

These results exclude an important role for either a circulating hormone or a reduction in plasma oncotic pressure in the natriuretic response to saline loading, and indicate that intrarenal factors are the critical determinants of the natriuresis. We have used the difference in response to saline loading in the immediate and delayed clamping experiments to evaluate the role of two intrarenal factors, interstitial hydrostatic pressure and renal plasma flow. Interstitial pressure changes were estimated from changes in tubular pressure and diameter by using the in situ compliance characteristics of the tubules. In a group of rats saline loaded without aortic clamping, interstitial pressure increased by 4-5 mm Hg and renal plasma flow increased by 2.5 ml/min. During the period of reduced renal artery pressure, however, neither interstitial pressure nor renal plasma flow was detectably increased above control in either the immediate or the delayed clamping experiments.

The only noteworthy difference between the experiments in which a natriuresis occurred (unclamped and delayed clamping studies) and the experiments in which no natriuresis occurred is that in the former group the kidney was at least transiently exposed both to an increase in renal plasma flow and interstitial pressure. These findings indicate, first, that extracellular fluid volume expansion can induce a natriuresis only if the kidney has been exposed to at least a transient increase in either interstitial hydrostatic pressure or renal plasma flow (or both); and, second, that a sustained increase in interstitial pressure and renal plasma flow is not required for the natriuresis to persist.

Full text

PDF
1428

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Barratt L. J., Wallin J. D., Rector F. C., Jr, Seldin D. W. Influence of volume expansion on single-nephron filtration rate and plasma flow in the rat. Am J Physiol. 1973 Mar;224(3):643–650. doi: 10.1152/ajplegacy.1973.224.3.643. [DOI] [PubMed] [Google Scholar]
  2. Bennett C. M. Effect of extracellular volume expansion upon sodium reabsorption in the distal nephron of dogs. J Clin Invest. 1973 Oct;52(10):2548–2555. doi: 10.1172/JCI107446. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Cortell S., Davidman M., Gennari F. J., Schwartz W. B. Catheter size as a determinant of outflow resistance and intrarenal pressure. Am J Physiol. 1972 Oct;223(4):910–915. doi: 10.1152/ajplegacy.1972.223.4.910. [DOI] [PubMed] [Google Scholar]
  4. Cortell S., Gennari F. J., Davidman M., Bossert W. H., Schwartz W. B. A definition of proximal and distal tubular compliance. Practical and theoretical implications. J Clin Invest. 1973 Sep;52(9):2330–2339. doi: 10.1172/JCI107422. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. DE WARDENER H. E., MILLS I. H., CLAPHAM W. F., HAYTER C. J. Studies on the efferent mechanism of the sodium diuresis which follows the administration of intravenous saline in the dog. Clin Sci. 1961 Oct;21:249–258. [PubMed] [Google Scholar]
  6. Daugharty T. M., Ueki I. F., Nicholas D. P., Brenner B. M. Comparative renal effects of isoncotic and colloid-free volume expansion in the rat. Am J Physiol. 1972 Jan;222(1):225–235. doi: 10.1152/ajplegacy.1972.222.1.225. [DOI] [PubMed] [Google Scholar]
  7. EARLEY L. E., FRIEDLER R. M. CHANGES IN RENAL BLOOD FLOW AND POSSIBLY THE INTRARENAL DISTRIBUTION OF BLOOD DURING THE NATRIURESIS ACCOMPANYING SALINE LOADING IN THE DOG. J Clin Invest. 1965 Jun;44:929–941. doi: 10.1172/JCI105210. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. GOTTSCHALK C. W., MYLLE M. Micropuncture study of pressures in proximal tubules and peritubular capillaries of the rat kidney and their relation to ureteral and renal venous pressures. Am J Physiol. 1956 May;185(2):430–439. doi: 10.1152/ajplegacy.1956.185.2.430. [DOI] [PubMed] [Google Scholar]
  9. Gennari F. J., Cortell S., Schwartz W. B. Loss of measured activity of inulin-14C and a corrective technique. J Appl Physiol. 1970 Jan;28(1):105–107. doi: 10.1152/jappl.1970.28.1.105. [DOI] [PubMed] [Google Scholar]
  10. Hebert L. A., Arbus G. S. Renal subcapsular pressure--a new intrarenal pressure measurement. Am J Physiol. 1971 Apr;220(4):1129–1136. doi: 10.1152/ajplegacy.1971.220.4.1129. [DOI] [PubMed] [Google Scholar]
  11. LEVINSKY N. G., LALONE R. C. THE MECHANISM OF SODIUM DURESIS AFTER SALINE INFUSION IN THE DOG. J Clin Invest. 1963 Aug;42:1261–1276. doi: 10.1172/JCI104811. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Lewy J. E., Windhager E. E. Peritubular control of proximal tubular fluid reabsorption in the rat kidney. Am J Physiol. 1968 May;214(5):943–954. doi: 10.1152/ajplegacy.1968.214.5.943. [DOI] [PubMed] [Google Scholar]
  13. Martino J. A., Earley L. E. Demonstraton of a role of physical factors as determinants of the natriuretic response to volume expansion. J Clin Invest. 1967 Dec;46(12):1963–1978. doi: 10.1172/JCI105686. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Stein J. H., Osgood R. W., Boonjarern S., Ferris T. F. A comparison of the segmental analysis of sodium reabsorption during Ringer's and hyperoncotic albumin infusion in the rat. J Clin Invest. 1973 Sep;52(9):2313–2323. doi: 10.1172/JCI107420. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Wolgast M., Persson E., Schnermann J., Ulfendahl H., Wunderlich P. Colloid osmotic pressure of the subcapsular interstitial fluid of rat kidneys during hydropenia and volume expansion. Pflugers Arch. 1973 May 18;340(2):123–131. doi: 10.1007/BF00588171. [DOI] [PubMed] [Google Scholar]

Articles from Journal of Clinical Investigation are provided here courtesy of American Society for Clinical Investigation

RESOURCES