Modulation of the renin-aldosterone system by iodotyrosines as tyrosine hydroxylase inhibitors.
This study shows that MIT and DIT stimulate aldosterone secretion. This may be due to their tyrosine hydroxylase inhibitory property. Dopamine abolishes the stimulation. Prolonged MIT administration enhances the stimulation of aldosterone secretion and can cause hypokalemia. Volume expansion reverses the hyperaldosteronism. PRA and blood pressure do not change, even after prolonged MIT intake.
Tan
S A
SA
Department of Medicine, Loma Linda University, California 92350.
Berk
L S
LS
Tan
L G
LG
D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D004105:Diiodotyrosine / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D006801:Humans; D006929:Hyperaldosteronism / Q000139:chemically induced; D007008:Hypokalemia / Q000139:chemically induced; D008297:Male; D007470:Monoiodotyrosine / Q000494:pharmacology*; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D014446:Tyrosine 3-Monooxygenase / Q000037:antagonists & inhibitors*
D000450:Aldosterone; D004105:Diiodotyrosine; D014446:Tyrosine 3-Monooxygenase; D007470:Monoiodotyrosine; D004298:Dopamine