Expression of the renal kallikrein gene in mineralocorticoid-treated and genetically hypertensive rats

• Published in: Journal of hypertension Vol. 4; no. 4; p. 427
• Main Authors: Fuller, P J, Clements, J A, Nikolaidis, I, Hiwatari, M, Funder, J W
• Format: Journal Article
• Language: English
• Published: England 01-08-1986
• Subjects: Animals; Female; Gene Expression Regulation - drug effects; Hypertension - genetics; Hypertension - metabolism; Kallikreins - biosynthesis; Kallikreins - genetics; Kidney - drug effects; Kidney - metabolism; Mineralocorticoids - pharmacology; Rats; Rats, Inbred SHR; Rats, Inbred Strains; Submandibular Gland - metabolism
• ISSN: 0263-6352
• DOI: 10.1097/00004872-198608000-00006

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.