Cardiovascular and analgesic effects of a highly palatable diet in spontaneously hypertensive and Wistar-Kyoto rats

Ingestion of highly palatable diets (HPDs), rich in sucrose and fat, has been shown to lead to obesity and alterations in cardiovascular function in animal models. A hypothesis has been advanced which suggests that ingestion of an HPD increases hypothalamic β-endorphin release, an effect which results in an increase in sympathetic nerve outflow during the development of obesity. The hypothesis was tested by chronic (10 weeks) feeding of male spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs) with the HPD or normal rat chow (ND). Cardiovascular function (systolic blood pressure, heart rate) and body weight gain were monitored during the feeding period. Pain sensitivity was tested weekly by measuring tail-flick latency. Body weight gain was greater in WKY rats than in SHRs, but ingestion of the HPD had no effect in either strain. Terminal organ analysis indicated differences between strains of SHRs and WKYs in the heart, the adrenal and pituitary glands, peritesticular fat pad, and testis weights expressed by organ weight/body weight. The heart weight was greater in SHRs on the HPD than in SHRs on the ND. The ingestion of the HPD significantly increased blood pressure only in SHRs, following 10 weeks of dietary intervention. However, tail-flick latency was prolonged in both SHRs and WKYs during ingestion of the HPD. Increases in tail-flick latency suggest that the HPD increases brain opiate levels in both SHRs and WKYs. Exaggerated increases in heart weight and blood pressure were noted in SHRs following feeding with the HPD, indicating enhanced sensitivity of SHRs to HPD-induced hypertension.