Following Skelton’s procedure with unilateral adrenonephrectomy, contralateral adrenal enucleation and application of 1 % NaCl with the drinking fluid, genetically normotensive rats develop hypertension and a generalized arteriosclerosis, i.e. necrotizing hypertensive angiopathy. In the present study, the effect of high blood pressure was investigated in 13 Skelton hypertensive rats and 13 normotensive control rats. Systolic blood pressure was investigated by tail plethysmography over a period of 7 weeks. During the experiments, 3 of the Skelton rats died with final high blood pressure values, whereas all controls remained alive. Mean systolic blood pressure of the 10 surviving Skelton rats increased from 108 to 223 mm Hg. The control rats remained normotensive. Accordingly, heart weights of the hypertensives were higher than those of the controls (p = 0.0027). At the end of the experiment, arteriosclerosis was quantified by counting the heart arteries and arterioles with deposits of fibrinoid in the vascular wall in 10 histological cross-sections per heart. In the right ventricular wall of 6 of the 10 surviving Skelton rats, arteries and arterioles with deposits of fibrinoid in the vascular wall were detected. No such alteration was observed in the left ventricular wall or in the interventricular septum. About one third of the altered blood vessels showed fibrinoid necrosis. In contrast, the normotensive control rats had neither fibrinoid necrosis nor sclerotic arteries in corresponding sections of the hearts (p = 0.0052). The findings show that Skelton hypertension can be used as an experimental model for quantitative histological investigation of coronary arteriosclerosis in hypertensive rats. It has to be carified why coronary arteriosclerosis only develops in the right and not in the left ventricular wall or in the interventricular myocardium, and why coronary arteriosclerosis is not obligatory in all hypertensive rats.