Recently we demonstrated that clonidine and moxonidine exert specific actio
n on fractional fluid and Nat excretion in anaesthetised Sprague-Dawley rat
s. Classically, most of the diuretics used induce an increased K+ excretion
, at least in part due to Nat load in the distal tubule and exchange of Na by K+. Therefore, we studied the effects of moxonidine and clonidine on K excretion in anaesthetised Sprague-Dawley rats. Moxonidine (0.25 and 0.5 m
g kg(-1) body wt, i.v.) increased transiently K+ (1.0 +/- 0.3-1.9 +/- 0.4 a
nd 0.9 +/- 0.2-2.9 + 0.7 mu mol min(-1) 100 g body wt.) and Na+ (1.4 +/- 1.
0-6.9 +/- 3.1 and 0.8 +/- 0.36-6.6 +/- 1.5 mu mol min(-1) 100 g body wt.) e
xcretion. Clonidine (0.25 mg kg-l) caused a more pronounced increase in K(1.0 +/- 0.1-2.7 +/- 0.4 mu mol min(-1) 100 g body wt.) and Na+ (0.6 +/- 0.
3-9.5 +/- 0.4 mu mol min(-1) 100 g body wt.) excretion, whereas the higher
dose of 0.5 mg kg-l body wt. had less effect as compared to moxonidine (K+:
0.8 +/- 0.1-1,7 +/- 0.2 mu mol min(-1) 100 g body wt., Na+: 0.3 +/- 0.1-3.
4 +/- 1.0 mu mol min(-1) 100 g body wt.). The increased electrolyte excreti
on returned (similar to moxonidine) to baseline levels within 20 min after
injection of the drugs. Antagonists such as idazoxan and yohimbine did not
change K+ and Na+ excretion by their own. Both, the non-selective imidazoli
ne/ alpha(2)-adrenoceptor antagonist idazoxan and the pure alpha(2)-adrenoc
eptor antagonist yohimbine attenuated the moxonidin-induced effects on K+ a
nd Na+ excretion. This could be also observed with clonidine and simultaneo
us injection of these two antagonists. Our results demonstrate that moxonid
ine and clonidine also increase renal K+ excretion in this animal model. K and Na+ excretion show a parallel behaviour, indicating that the increased
K+ excretion is mainly due to Na+ load in the tubular system. (C) 1999 Aca
demic Press.