Key result
Infusion of angiotensin I or II and administration of enalapril did not increase urinary angiotensin excretion despite massive increases in plasma levels, suggesting an intrarenal origin.
Why the study?
Does plasma angiotensin concentration, ACE inhibition, or sodium intake affect urinary angiotensin excretion in healthy humans?
Population
15 healthy subjects (7 in the angiotensin infusion study, 8 in the enalapril/sodium intake study)
Comparison
Intravenous infusion of angiotensin I or… vs Baseline levels prior to infusion or enalapril…
Authors
Loading...
Urinary ANG excretion may not track plasma levels in healthy subjects; leaves open its value as a renal biomarker.
Does plasma angiotensin concentration, ACE inhibition, or sodium intake affect urinary angiotensin excretion in healthy humans?
Urinary angiotensin I and II appear to originate from an intrarenal source rather than from plasma filtration, as their excretion is independent of plasma levels, sodium intake, and ACE inhibition.
Vos et al. (1994) studied Healthy (n=15). Angiotensin I or II infusion and enalapril administration vs. Baseline was evaluated on Urinary ANG I and ANG II excretion. Infusion of angiotensin I or II and administration of enalapril did not increase urinary angiotensin excretion despite massive increases in plasma levels, suggesting an intrarenal origin.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: