Acute and long‐term effects of aldosterone on vascular remodeling

We have previously demonstrated that aldosterone‐induced upregulation of cyclooxygenase (COX) expression in the kidney is blocked by eplerenone. The objective of this study was to determine whether ALDO causes biochemical and molecular remodeling of the vasculature. The effects of aldosterone on arachidonic acid metabolism and on the expression of thromboxane (TXA2) receptor (TP) were evaluated in the Dahl salt sensitive (DS) rat aorta, renal, femoral and carotid arteries. DS rats on a low salt (0.3% NaCl) diet were treated with or without ALDO for four weeks. Indirect blood pressure (BP), the release of TXA2, prostacyclin (PGI2) and prostaglandin E2, and the expression of COX‐2 and TP were measured. ALDO increased BP (17± 1%) and the basal release of PGE2 but reduced the basal release of TXA2. ALDO enhanced vascular reactivity to phenylephrine and up regulated the expression of COX‐2 in both aorta and renal vessels but reduced COX‐2 expression in the femoral artery. The TP expression was down regulated in the aorta but up regulated in the carotid by ALDO. These data reveal that the effect of ALDO in the vasculature is tissue specific and involves the release of vasoconstrictor prostanoids in the rat aorta by up regulating the expression of COX‐2 and TP in the vasculature. Therefore, it can be stated that the prostanoids play a pivotal role in the vasculopathic effect of aldosterone. Supported by NIDDK grant 1SC1DK082385.