In previous works, cicletanine has proven a protective effect on tissues in stroke-prone spontaneously hypertensive rats. The mechanism by which cicletanine lessens the tissue lesion incidence may be explained by the direct vascular effect of increased prostacyclin synthesis and by interaction with various agents mobilizing intracellular. Ca2+ ions. Histological so as to ultrastructural studies of the capillaries and small arteries were performed, specially on those of brain, kidney, heart, and choroid. Method : 36 SHR-SP/A 3N Iffa Credo rats aged 11 weeks were divided into 3 groups. Their drinking water was added with 1 p. 100 NaCl in. Group I was a control group, groups II and III were orally treated with cicletanine, respectively 100 and 150 mg/Kg. Systolic blood pressure, body weight, survival were reported. After 7 weeks of treatment the surviving rats were sacrificed. RESULTS the control group arterioles showed endoluminal debris with intimal proliferation and a large disorganisation of the media with adventitial fibrosis. The treated groups only showed a slight oedema of the subendothelial space in ultrastructure with no intimal proliferation and no muscle coat disorganisation or proliferation. CONCLUSIONS even though the decrease in blood pressure turned out to be very unimportant, the amount of lesions in vessels was striking even when treatment had been started on a already high blood pressure. The vessel walls only presented the impairments usually observed in early arterial response to hypertension. This study shows that cicletanine, due to its properties to increase PG12 synthesis and counterbalance the increase of cytosolic free Ca2+, improves the normal course of hypertensive vascular lesions in the SHR-SP.