Endocrine Abstracts

Arterial hypertension usually results from the deregulation and hyperactivity of the renin angiotensin-aldosterone system. One of the available therapeutic approaches for its treatment is the use of mineralocorticoid receptor (MR) antagonists, thus blocking aldosterone action.

The aim of this study was to characterize the effects of spironolactone and eplerenone, on the morphology of the adrenal gland of spontaneously hypertensive (SHR) and normotensive (Wistar-Kyoto) rats.

SHR (n=18) and Wistar-Kyoto (n=18) rats were exposed, for 1 month, to spironolactone (100 mg/kg per day, n=6), eplerenone (50 mg/kg per day, n=6) or not exposed to either drug (n=6) and at the end of this period their adrenal glands were collected and we evaluated the percentage of the stained area (%SA) of CyP11B1, CyP11B2, the adrenal inner zone antibody (IZAb), a proliferation marker (ki-67), β-catenin and finally the percentage of cellular area occupied by lipid droplets as well as the capsular width.

SHR Hypertensive rats presented higher area of lipid droplets in all layers of the adrenal cortex, an effect that was even further increased by the exposure to eplerenone, in the fasciculata and reticularis zones. In the normotensive rats it was only spironolactone that elicited this effect, being significant only in zona reticularis. Both drugs also increased Ki-67 expression in the hypertensive rats, but only eplerenone increased it on normotensive rats. Finally, spironolactone decreased the capsular size but only in the normotensive rats. No significant differences were found for the % SA of CyP11B1, CyP11B2, IZAb or β-catenin.

In conclusion, we have found that, morphologically the adrenal glands of normotensive and SHR only differed in number of lipid droplets. Exposure to the MR antagonists had significant consequences on the capsular size, lipidic depots and on the cellular proliferation of both normotensive and SHR adrenal glands.