CGP48369 is a potent angiotensin II receptor antagonist with antihypertensive effects that enhances endothelium-dependent relaxation of coronary arteries in spontaneously hypertensive rats.

Binding to the AT1 receptor (IC50 1.8 nM in vascular smooth muscle cells, VSMC), CGP 48369 inhibits AII-induced contraction in rabbit aorta (IC50 8.7 nM)[2].

In two-kidney/one-clip renal hypertensive rats, CGP48369 (10 mg/kg/day p.o.) reduces blood pressure for at least 24 h. In arteries with endothelium, contractions induced by AII at 3×10-8 M do not differ between untreated spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. However, significantly smaller contractions are observed in SHR treated with CGP48369 compared to the other treated SHR groups. Antihypertensive treatment with benazepril or nifedipine, and to a lesser extent with CGP48369, increases sensitivity (pD2-value) to intraluminal ACh. In arteries without endothelium, sensitivity to NE is identical in all groups, while the maximal response in CGP48369-treated SHR and nifedipine-treated SHR is slightly greater compared to that in WKY[1]. In SHR, antihypertensive therapy with benazepril HCl, CGP48369, valsartan, or nifedipine (each 10 mg/kg/day for 8 weeks) significantly increases endothelium-dependent relaxations evoked by acetylcholine[1].