Related Experiment Videos
Acute hypoxia and endogenous renal endothelin
A Nir1, A L Clavell, D Heublein
1Department of Pediatrics, Mayo Clinic and Foundation, Rochester, MN.
Summary
Acute moderate hypoxia increases urinary endothelin (ET) excretion and renal tubular ET immunoreactivity. This suggests endothelin plays a role in regulating kidney sodium balance during hypoxia.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Renal Physiology
Background:
- Endothelin (ET) is a potent vasoconstrictor peptide.
- Emerging evidence suggests nonvascular roles for ET in the kidney.
- The renal response to hypoxia requires further elucidation.
Purpose of the Study:
- To investigate the renal endothelin (ET) response to acute moderate hypoxia.
- To assess changes in urinary ET excretion and renal tissue ET immunoreactivity.
- To correlate these ET changes with hemodynamic and excretory alterations during hypoxia.
Main Methods:
- Anesthetized dogs were subjected to either hypoxic (10% O2) or normoxic ventilation for 60 minutes.
- Urinary ET excretion, urine flow, and sodium excretion were measured.
- Renal tissue was analyzed for ET immunoreactivity using immunohistochemistry.
Main Results:
- Hypoxia significantly increased urinary ET excretion, urine flow, and sodium excretion.
- No significant changes were observed in GFR, RBF, renal vascular resistance, or mean arterial pressure.
- Increased ET staining was noted in renal tubules of the hypoxic group.
Conclusions:
- Acute moderate hypoxia elevates urinary ET excretion and renal tubular ET immunoreactivity.
- These findings suggest a nonvascular role for renal endothelin in sodium homeostasis during hypoxia.
- Endogenously produced renal ET may regulate sodium balance under hypoxic conditions.