Background:

Potassium canrenoate is a competitive antagonist of aldosterone receptor [1].

Aldosterone is a steroid hormone and plays an important role in the regulation of blood pressure by increasing reabsorption of ions and water in the kidney.

In cultured rat and human cells, potassium canrenoate produced genotoxic effects in a doce-dependant way [2].

In male Wistar rats injected with isoprenaline (400 mg/kg), heart and left ventricular weights increased significantly. While potassium canrenoate (20 mg/kg/day) relieved this increase. Potassium canrenoate significantly reduced the fibrosis induced by isoprenaline [1]. In 30 essential hypertensives, canrenoate potassium reduced intraerythrocyte Na+ content and increased Na-K pump [3]. In 15 patients with idiopathic primary aldosteronism, potassium canrenoate normalized the aldosterone/plasma renin activity (PRA) ratio [4].

参考文献:
[1].  Bos R, Mougenot N, Médiani O, et al. Potassium canrenoate, an aldosterone receptor antagonist, reduces isoprenaline-induced cardiac fibrosis in the rat. J Pharmacol Exp Ther, 2004, 309(3): 1160-1166.
[2].  Martelli A, Mattioli F, Carrozzino R, et al. Genotoxicity testing of potassium canrenoate in cultured rat and human cells. Mutagenesis, 1999, 14(5): 463-472.
[3].  Niutta E, Cusi D, Colombo R, et al. Antihypertensive effect of captopril, canrenoate potassium, and atenolol. Relations with red blood cell sodium transport and renin. Am J Hypertens, 1988, 1(4 Pt 1): 364-371.
[4].  Armanini D, Scaroni C, Mattarello MJ, et al. Idiopathic primary hyperaldosteronism: normalization of plasma aldosterone after one month withdrawal of long-term therapy with aldosterone-receptor antagonist potassium canrenoate. J Endocrinol Invest, 2005, 28(3): 236-240.