Humoral determinants of Na+ excretion after intravenous NaCl loading in normal volunteers

• Published in: Clinical and experimental pharmacology & physiology Vol. 20; no. 5; p. 310
• Main Authors: Stokes, G S, Johnston, H J, Monaghan, J C
• Format: Journal Article
• Language: English
• Published: Australia 01-05-1993
• Subjects: Adolescent; Adult; Aldosterone - blood; Aldosterone - urine; Atrial Natriuretic Factor - blood; Carbidopa - administration & dosage; Carbidopa - pharmacology; Dopamine - urine; Female; Humans; Indomethacin - administration & dosage; Indomethacin - pharmacology; Kallikreins - urine; Male; Middle Aged; Natriuresis - drug effects; Norepinephrine - urine; Prostaglandins - urine; Prostaglandins E - urine; Renin - blood; Serum Albumin - analysis; Sodium - administration & dosage; Sodium - urine
• ISSN: 0305-1870
• DOI: 10.1111/j.1440-1681.1993.tb01691.x

1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order). 2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3-fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGE2) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa-treated subjects and in three out of six indomethacin-treated subjects, but showed little or no change in the remainder. 3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin-dependent or dopamine-dependent mechanisms for Na+ excretion.