INTRODUCTIONLow erucic acid rapeseed (canola) oil (CO) has been reported to shorten survival times in stroke-prone spontaneously hypertensive rats (SHRSP), compared with rats given soybean oil (SO), when each oil was added at 10 w/w% to standard rat chow (Huang et al., , 1997Miyazaki et al., 1998). Previous studies suggested that CO ingestion shortens the life of SHRSP via an acceleration of hypertension-related conditions, including elevation of blood pressure and tissue lesions in the kidney and heart (Naito et al., 2003;Ohara et al., 2006). On the other hand, it was found that CO ingestion elevated blood pressure and plasma lipids and caused vascular lesions not only in SHRSP but in spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats (Naito et al., 2000a(Naito et al., , 2000b. However, such unfavorable effects have been found exclusively in SHRSP and its closely related strains, and there have been no reports on CO-induced effects using rats of other strains. Therefore, the present study examined whether or not such unfavorable effects of CO are restricted to SHRSP and its related strains. For this purpose Wistar rats, the strain from which WKY rats, SHR and SHRSP were derived, were fed a diet containing 10 w/w% CO as the sole fat nutrient for 10 weeks, and the resulting changes in clinical signs were compared with those in control rats fed SO instead of CO.
MATERIALS AND METHODS
Animals and breedingSixteen male Wistar rats, 4 weeks old, were purchased ABSTRACT -Dietary rapeseed (canola) oil (CO) given as the only fat nutrient shortens life in strokeprone spontaneously hypertensive rats (SHRSP), compared with SHRSP given soybean oil (SO) instead of CO. CO ingestion increases plasma lipids and causes renal lesions in SHRSP and in spontaneously hypertensive rats (SHR), and increases plasma lipids also in Wistar Kyoto (WKY) rats, a normotensive counterpart of SHR. This study examined whether or not such unfavorable effects of CO are restricted to these closely related strains. For this purpose Wistar rats, the strain from which these strains were derived, were fed a diet containing 10% CO or SO as the sole fat nutrient for 10 weeks, and changes in clinical signs, urinalysis, blood biochemistry and pathology were compared. CO ingestion did not induce Na + , compared with the SO group. Thus, the unfavorable effects of CO ingestion appear to be restricted to SHRSP and its closely related strains. The role of increased aldosterone and Na + in the unfavorable events caused by CO in SHRSP, SHR and WKY rats, and any factors which could induce such increases in aldosterone and Na + , remain to be elucidated.