Mineralocorticoid escape during kallikrein inhibition.
Kinins have been considered to be involved in the escape from the sodium retaining effects of mineralocorticoids. In a metabolic study in rats, the importance of the kallikrein-kinin system for sodium and potassium excretion was evaluated by aprotinin-induced kallikrein inhibition under basal conditions and during DOCA administration. Kallikrein inhibition was accompanied by a transient sodium retention. The escape from the sodium retaining effect of DOCA was not affected. However, the DOCA-induced potassium loss was enhanced. Kallikrein inhibition decreased urinary prostaglandin (PG) E2 and prevented the DOCA-induced rise in PGE2. Plasma renin activity was stimulated after 10 days of aprotinin administration. The kallikrein-kinin system is not an important mediator of the escape phenomenon but it may play a role in the regulation of sodium and potassium excretion.
A
A
Overlack
E
E
Bäcker-Kreutz
C
C
Ressel
H M
HM
Müller
R
R
Kolloch
K O
KO
Stumpe
D000818:Animals; D007611:Aprotinin / Q000378:metabolism*; D003900:Desoxycorticosterone / Q000378:metabolism*; D015232:Dinoprostone; D007610:Kallikreins / Q000652:urine; D008297:Male; D011188:Potassium / Q000378:metabolism; D011458:Prostaglandins E / Q000652:urine; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism
D011458:Prostaglandins E; D003900:Desoxycorticosterone; D007611:Aprotinin; D012964:Sodium; D007610:Kallikreins; D012083:Renin; D015232:Dinoprostone; D011188:Potassium