HUMORAL DETERMINANTS OF Na+EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS
Autor: | G. S. Stokes, H. J. Johnston, J. C. Monaghan |
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Rok vydání: | 1993 |
Předmět: |
Adult
Male medicine.medical_specialty Adolescent Physiology Dopamine Urinary system medicine.medical_treatment Indomethacin Natriuresis Pharmacology Plasma renin activity Excretion Norepinephrine chemistry.chemical_compound Atrial natriuretic peptide Physiology (medical) Internal medicine Renin medicine Humans Aldosterone Saline Serum Albumin Chemistry Prostaglandins E Sodium Carbidopa Middle Aged Endocrinology Prostaglandins Female Kallikreins Atrial Natriuretic Factor medicine.drug |
Zdroj: | Clinical and Experimental Pharmacology and Physiology. 20:310-312 |
ISSN: | 1440-1681 0305-1870 |
DOI: | 10.1111/j.1440-1681.1993.tb01691.x |
Popis: | SUMMARY 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 and 13.00h 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 (PGEI) 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. |
Databáze: | OpenAIRE |
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