Influence of captopril on renal hemodynamics and segmental tubular reabsorption of sodium in humans.
Acute angiotensin-converting enzyme inhibitors (ACEIs) have been found to induce natriuresis in humans as well as in experimental animals. However, the tubular sites involved have not been precisely evaluated in humans. Using both free-water and lithium clearance, the latter as a marker of proximal tubular reabsorption, we measured segmental tubular movement of sodium before and after acute captopril administration in eight healthy normotensive volunteers on normal sodium diet. Captopril decreased slightly but significantly glomerular filtration rate (GFR), filtration fraction, and mean arterial pressure (MAP), whereas renal plasma flow (RPF) was unchanged. Captopril acutely increased excretion rate and fractional excretion of sodium. When assessed by lithium clearance, both absolute and fractional proximal reabsorption of sodium and fractional distal reabsorption of sodium were found to be decreased by captopril. When assessed by free-water clearance, both fractional proximal and distal reabsorption of sodium were found to be decreased by captopril but only the decrease in fractional proximal reabsorption was significant. These results indicate that captopril-induced natriuretic effect is due to decreased sodium reabsorption in both proximal and distal sites of the nephron. Shifts in segmental tubular sodium reabsorption obtained from either free-water or lithium clearance are directionally similar but quantitatively different. Results obtained from lithium clearance indicate that the rate of fluid delivery to the diluting segment is at least twice as great as that estimated from free-water calculations. Lithium clearance techniques therefore appear to be more sensitive in detecting subtle changes in segmental tubular reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)
Hannedouche
T
T
Department of Nephrology, Necker Hospital, Paris, France.
Delgado
A
A
Gnionsahe
A
A
Lacour
B
B
Grunfeld
J P
JP
D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D001834:Body Water / Q000378:metabolism; D002216:Captopril / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism*; D008094:Lithium / Q000652:urine; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D012079:Renal Circulation / Q000187:drug effects*; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000378:metabolism
D012965:Sodium Chloride; D008094:Lithium; D002216:Captopril; D012964:Sodium; D007703:Peptidyl-Dipeptidase A