Electrolyte Blood Press.  2010 Jun;8(1):10-17. 10.5049/EBP.2010.8.1.10.

Is There Escape from Renal Actions of Vasopressin in Rats with a Hyponatremia for Greater than 48 Hours?

Affiliations
  • 1Renal Divisions, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada. mitchell.halperin@utoronto.ca
  • 2Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada.

Abstract

Escape from the renal actions of vasopressin is said to occur in rats with chronic hyponatremia. Our objective was to provide specific evidence to test this hypothesis. Hence the osmolality in the excised renal papilla and in simultaneously voided urine (U(Osm)) was measured in rats with and without hyponatremia. To induce hyponatremia, rats were fed low-electrolyte chow for 6 days. In the first 3 days, water was provided ad lib. On days 4 to 6, a long acting vasopressin preparation (dDAVP) was given every 8 hours to induce water retention. The hyponatremic rats drank 21 mL 5% sucrose on day 4 and 6 mL on day 5. On the morning of day 6, these rats were given 10 mL of 5% glucose in water (D5W) by the intraperitoneal route at 09:00 hour and at 11:00 hour. Analyses were performed in blood, urine, and the excised renal papilla at 13:00 hour on day 6. The concentration of Na+ in plasma (P(Na)) in rats without intraperitoneal D5W was 140+/-1 mEq/L (n=7) whereas it was 112+/-3 mEq/L in the hyponatremic group (n=12). The hyponatremic rats had a higher osmolality in the excised papillary (1,915+/-117 mOsm/kg H2O) than the U(Osm) (1,528+/-176 mOsm/kg H2O, P<0.05). One explanation for this difference is that the rats escaped from the renal action of vasopressin. Nevertheless, based on a quantitative analysis, other possibilities will be considered.

Keyword

vasopressins; aquaporins; basal water permeability; concentration of the urine

MeSH Terms

Animals
Aquaporins
Glucose
Hyponatremia
Osmolar Concentration
Plasma
Rats
Retention (Psychology)
Sucrose
United Nations
Vasopressins
Water
Aquaporins
Glucose
Sucrose
Vasopressins
Water

Reference

1. Ecelbarger CA, Nielsen S, Olson BR, et al. Role of renal aquaporins in escape from vasopressin-induced antidiuresis in rat. J Clin Invest. 1997; 99:1852–1863. PMID: 9109429.
Article
2. Ecelbarger CA, Chou CL, Lee AJ, DiGiovanni SR, Verbalis JG, Knepper MA. Escape from vasopressin-induced antidiuresis: role of vasopressin resistance of the collecting duct. Am J Physiol. 1998; 274:F1161–F1166. PMID: 9841509.
3. Ecelbarger CA, Knepper MA, Verbalis JG. Increased abundance of distal sodium transporters in rat kidney during vasopressin escape. J Am Soc Nephrol. 2001; 12:207–217. PMID: 11158210.
Article
4. Hoorn EJ. Water and salt: from renal mechanisms to clinical disorders [dissertation]. 2007. Rotterdam: Erasmus Universiteit Rotterdam.
5. Murase T, Tian Y, Fang XY, Verbalis JG. Synergistic effects of nitric oxide and prostaglandins on renal escape from vasopressin-induced antidiuresis. Am J Physiol Regul Integr Comp Physiol. 2003; 284:R354–R362. PMID: 12388460.
6. Murase T, Ecelbarger CA, Baker EA, Tian Y, Knepper MA, Verbalis JG. Kidney aquaporin-2 expression during escape from antidiuresis is not related to plasma or tissue osmolality. J Am Soc Nephrol. 1999; 10:2067–2075. PMID: 10505682.
Article
7. Song J, Hu X, Khan O, Tian Y, Verbalis JG, Ecelbarger CA. Increased blood pressure, aldosterone activity, and regional differences in renal ENaC protein during vasopressin escape. Am J Physiol Renal Physiol. 2004; 287:F1076–F1083. PMID: 15226153.
Article
8. Verbalis JG. Escape from antidiuresis: a good story. Kidney Int. 2001; 60:1608–1610. PMID: 11576381.
Article
9. Tian Y, Sandberg K, Murase T, Baker EA, Speth RC, Verbalis JG. Vasopressin V2 receptor binding is down-regulated during renal escape from vasopressin-induced antidiuresis. Endocrinology. 2000; 141:307–314. PMID: 10614652.
10. Gowrishankar M, Lenga I, Cheung RY, Cheema-Dhadli S, Halperin ML. Minimum urine flow rate during water deprivation: importance of the permeability of urea in the inner medulla. Kidney Int. 1998; 53:159–166. PMID: 9453013.
Article
11. Cheema-Dhadli S, Halperin ML. Relative rates of appearance of nitrogen and sulphur: implications for postprandial synthesis of proteins. Can J Physiol Pharmacol. 1993; 71:120–127. PMID: 8319135.
Article
12. Halperin ML, Vinay P, Gougoux A, Pichette C, Jungas RL. Regulation of the maximum rate of renal ammoniagenesis in the acidotic dog. Am J Physiol. 1985; 248:F607–F615. PMID: 3985167.
Article
13. Gamble J, McKhann C, Butler A, Tuthill E. An economy of water in renal function referable to urea. Am J Physiol. 1934; 109:139–154.
Article
14. Steele A, deVeber H, Quaggin SE, Scheich A, Ethier J, Halperin ML. What is responsible for the diurnal variation in potassium excretion? Am J Physiol. 1994; 267:R554–R560. PMID: 8067468.
Article
15. Schmidt-Nielsen B, Churchill M, Reinking LN. Occurrence of renal pelvic refluxes during rising urine flow rate in rats and hamsters. Kidney Int. 1980; 18:419–431. PMID: 7230608.
Article
16. Robinson AG, Roberts MM, Evron WA, Verbalis JG, Sherman TG. Hyponatremia in rats induces downregulation of vasopressin synthesis. J Clin Invest. 1990; 86:1023–1029. PMID: 2211999.
Article
17. Hoorn EJ, Hoffert JD, Knepper MA. Combined proteomics and pathways analysis of collecting duct reveals a protein regulatory network activated in vasopressin escape. J Am Soc Nephrol. 2005; 16:2852–2863. PMID: 16079266.
Article
Full Text Links
  • EBP
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr