Expression of the renal kallikrein gene in mineralocorticoid-treated and genetically hypertensive rats.
On the basis of both clinical observations and experimental studies it has been proposed that renal kallikrein is a mineralocorticoid regulated protein. In other studies, changes in renal kallikrein activity have been implicated in the genesis of, and/or response to, hypertension. Using a cloned complementary DNA (cDNA) to rat pancreatic kallikrein (pcXP39) for hybridization histochemistry, and both Northern and dot blot analysis, we studied expression of the kallikrein gene in steroid-treated control animals, and in three strains of genetically hypertensive rats. No differences in renal kallikrein messenger RNA (mRNA) levels were found between adrenalectomized rats and those treated for 5-14 days with 9 alpha-fludrocortisone, corticosterone or dexamethasone, or between hypertensive rats and their appropriate controls. Since mRNA levels appear essentially invariant under such circumstances, the change in renal kallikrein activity/immunoreactivity after chronic mineralocorticoid elevation, or in hypertensive rats, presumably reflects modulation at the post-transcriptional level.
D000818:Animals; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism; D007610:Kallikreins / Q000096:biosynthesis / Q000235:genetics*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008901:Mineralocorticoids / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D013363:Submandibular Gland / Q000378:metabolism
D008901:Mineralocorticoids; D007610:Kallikreins