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Action of compounds with effective in vivo mineralocorticoid activity on ion transport in leucocytes.
Author(s) -
Baron DN,
Green RJ
Publication year - 1986
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1986.tb02819.x
Subject(s) - carbenoxolone , aldosterone , endocrinology , fludrocortisone , mineralocorticoid , ouabain , medicine , chemistry , in vivo , efflux , propranolol , sodium , hydrocortisone , biology , biochemistry , intracellular , microbiology and biotechnology , organic chemistry , gap junction
We have studied the in vitro short‐term effects of aldosterone (1.0‐ 1000 nmol l‐1), cortisol (0.5‐5.0 mumol l‐1), fludrocortisone (1.0‐10 nmol l‐1) and carbenoxolone (0.5‐3 mmol l‐1) on 86rubidium influx (a model for potassium), 22sodium efflux, and [3H]‐ouabain binding capacity in intact human leucocytes. No effect of aldosterone (at concentrations present in Conn's syndrome) or fludrocortisone could be demonstrated on cation fluxes or [3H]‐ouabain binding compared to controls. No significant effect of cortisol, at concentrations either physiological or present in Cushing's syndrome, could be demonstrated on cation fluxes or [3H]‐ouabain binding compared to controls. Carbenoxolone significantly increased 86Rb influx and 22Na efflux at concentrations known to cause hypokalaemia in man. The effect was not blocked by propranolol. No effect could be demonstrated for [3H]‐ ouabain binding.