Acute vascular effect of aldosterone on mesenteric artery from normal and heart failure rats

Numerous evidences have emerged in resent years to support the direct role of aldosterone in heart failure. This study was designed to test our hypothesis that, the vascular response to aldosterone alters in a situation of heart failure. Acute heart failure of rat was induced by coronary artery ligation for 30 min. Segments of third‐order branches of the mesenteric artery were isolated for isometric tension recording. We found that in normal rats, aldosterone (10 −9 M ‐ 10 −6 M) caused further contraction in mesenteric artery precontracted by phenylephrine (PE, 10 −6 mol/L), but aldosterone did not cause vasocontraction in the artery from heart failure rats. In the mesenteric artery from normal rats, pre‐incubation of aldosterone (3×10 −7 M) for 10 min decreased the contractile response to low concentration of PE (1×10 −7 ‐ 1×10 −6 M), but enhanced the contractile response to high concentration of PE (3×10 −6 ‐ 3×10 −5 M). This effect was abolished by eplerenone (2×10 −6 M), an inhibitor of aldosterone receptor. However, in the artery from heart failure rats, aldosterone (3×10 −7 M) decreased the contraction induced by PE (1×10 −7 ‐ 3×10 −5 M), which was partly blocked by eplerenone. These results indicate that aldosterone has biphasic effect on contractile response to PE of normal rat artery, mediated by aldosterone receptor. The effect of aldosterone on heart failure rat artery is monophasic, reducing the sensitivity to PE, which is partly mediated by aldosterone receptor.