A micropuncture study of potassium excretion by the remnant kidney
- PMID: 4703232
- PMCID: PMC302413
- DOI: 10.1172/JCI107322
A micropuncture study of potassium excretion by the remnant kidney
Abstract
In order to study the mechanism of enhanced potassium excretion by the remaining nephrons of the remnant kidney, micropuncture and clearance experiments were carried out in rats after surgical ablation of 3/4 of the total renal mass. The potassium intake in all animals was approximately 5 meq/day. Animals were studied 24 h and 10-14 days after 3/4 nephrectomy. Balance measurements in the chronic animals before micropuncture study indicated that 24 h K(+) excretion by the remnant kidney was equal to that of the two kidneys before ablation of renal mass. Measurements of distal tubular inulin and potassium concentrations revealed progressive reabsorption of potassium in this segment of the nephron in both the 24-h and chronic 3/4-nephrectomized rats, as well as in normal control rats. A large increase in tubular fluid potassium content occurred between the end of the distal tubule and the final urine in the 3/4-nephrectomized rats, but not in the normal controls. These observations suggest that the segment of the nephron responsible for enhanced potassium excretion by remaining nephrons was the collecting duct. In additional experiments, potassium was completely eliminated from the diet of chronic 3/4-nephrectomized rats before micropuncture study. In these animals, no addition of K(+) occurred beyond the distal tubules. Normal rats infused with 0.15 M KCl to acutely elevate serum K(+) concentration, demonstrated reabsorption of K(+) in the distal tubule and a large addition of K(+) to the urine beyond the distal tubule. We conclude that the collecting duct is the major site of regulation of urinary potassium excretion in normal rats and is responsible for the adaptation to nephron loss by the remnant kidney.
Similar articles
-
A micropuncture study of renal phosphate transport in rats with chronic renal failure and secondary hyperparathyroidism.J Clin Invest. 1978 Apr;61(4):884-94. doi: 10.1172/JCI109014. J Clin Invest. 1978. PMID: 659581 Free PMC article.
-
Effects of acute unilateral renal denervation in the rat.J Clin Invest. 1975 Jul;56(1):208-17. doi: 10.1172/JCI108069. J Clin Invest. 1975. PMID: 1141432 Free PMC article.
-
Micropuncture study of water, electrolytes, and urea movements along the loops of henle in psammomys.J Clin Invest. 1969 Mar;48(3):474-86. doi: 10.1172/JCI106005. J Clin Invest. 1969. PMID: 5773086 Free PMC article.
-
Functional adaptation to reduction in renal mass.Physiol Rev. 1979 Jan;59(1):137-64. doi: 10.1152/physrev.1979.59.1.137. Physiol Rev. 1979. PMID: 220646 Review.
-
Renal potassium transport: contributions of individual nephron segments and populations.Am J Physiol. 1978 Dec;235(6):F515-27. doi: 10.1152/ajprenal.1978.235.6.F515. Am J Physiol. 1978. PMID: 367178 Review.
Cited by
-
Chronic reduction in renal mass: micropuncture studies of response to volume expansion and furosemide.Yale J Biol Med. 1978 May-Jun;51(3):289-95. Yale J Biol Med. 1978. PMID: 735151 Free PMC article.
-
Structural and functional adaptation after reduction of nephron population.Yale J Biol Med. 1979 May-Jun;52(3):271-87. Yale J Biol Med. 1979. PMID: 380185 Free PMC article. Review.
-
Some reflections on the mechanism of renal tubular potassium transport.Yale J Biol Med. 1975 Sep;48(4):315-36. Yale J Biol Med. 1975. PMID: 1202761 Free PMC article.
-
A functional comparison of the cortical collecting tubule and the distal convoluted tubule.J Clin Invest. 1975 Jun;55(6):1284-94. doi: 10.1172/JCI108048. J Clin Invest. 1975. PMID: 1133174 Free PMC article.
-
Acute compensatory adaptation of renal function following contralateral kidney exclusion in Brattleboro rats with diabetes insipidus.J Physiol. 1978 Oct;283:425-38. doi: 10.1113/jphysiol.1978.sp012510. J Physiol. 1978. PMID: 722584 Free PMC article.
References
MeSH terms
Substances
LinkOut - more resources
Full Text Sources