HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.

Abstract
Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P < 0.05) because of hyperventilation (arterial PCO2 25.6 +/- 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.
AuthorsClaudia Höhne, Willehad Boemke, Nora Schleyer, Roland C Francis, Martin O Krebs, Gabriele Kaczmarczyk
JournalJournal of applied physiology (Bethesda, Md. : 1985) (J Appl Physiol (1985)) Vol. 92 Issue 5 Pg. 2097-104 (May 2002) ISSN: 8750-7587 [Print] United States
PMID11960962 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Bicarbonates
  • Chlorides
  • Sodium, Dietary
  • Angiotensin II
  • Lactic Acid
  • Aldosterone
  • Atrial Natriuretic Factor
  • Sodium
  • Potassium
  • Calcium
Topics
  • Aldosterone (blood)
  • Alkalosis, Respiratory (metabolism)
  • Angiotensin II (blood)
  • Animals
  • Arteries (physiology)
  • Atrial Natriuretic Factor (blood)
  • Bicarbonates (blood, urine)
  • Blood Gas Analysis
  • Calcium (blood)
  • Chlorides (blood)
  • Dogs
  • Female
  • Hemodynamics (physiology)
  • Hydrogen-Ion Concentration
  • Hypoxia (metabolism)
  • Kidney (metabolism)
  • Kidney Function Tests
  • Lactic Acid (blood)
  • Osmolar Concentration
  • Potassium (blood, urine)
  • Sodium (blood, urine)
  • Sodium, Dietary

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: