CATECHOLAMINES ARE REQUIRED FOR ANDROGEN-INDUCED ODC EXPRESSION BUT NOT FOR HYPERTROPHY OF MOUSE KIDNEY

Catecholamine depletion, evoked by reserpine, dramatically impaired (f i-fold) the testosterone-induced increase of ornithine decarboxylase ( ODC) activity in female mouse kidney. However, reserpine did not preve nt kidney hypertrophy evoked by testosterone. This is evidenced by the activity of sensitive, biochemical markers of renal hypertrophy. name ly arginase and ornithine aminotransferase (OAT), that responded with the increase and decrease of activities to testosterone treatment, res pectively [1]. Arginine and ornithine, substrates and/or products of m arker enzymes, showed a striking homeostasis as their level was not af fected by testosterone and reserpine, and only slightly by DFMO. North ern blot analysis revealed that the ODC mRNA level, that was increased 10-fold by testosterone. was decreased 2-fold in catecholamine-deplet ed hypertrophic kidney. Thus, ODC transcript level, lowered by reserpi ne, correlated partially with an attenuated response of ODC activity t o testosterone. This was in contrast to DFMO. which inhibited ODC acti vity. but significantly increased its mRNA content. It is concluded th at catecholamines could be involved together with testosterone in regu lation of the ODC gene expression in mouse kidney. (C) 1997 Elsevier S cience B.V.