Caloric restriction and blood pressure regulation during metabolic syndrome

Poor dietary practices such as excessive glucose, sodium, and saturated fat intake are well-established contributing factors to promoting hypertension. Additionally, the obesity associated with the metabolic syndrome (MetS) is considered a significant contributing factor to the develop of the MetS-associated hypertension. Conversely, behavioral modifications of diet such as caloric restriction (CR) and intermittent fasting contribute to significant loss of body mass through reduced adiposity, which can lead to a decrease in arterial pressure. CR in combination with other behavioral modifications such as physical activity is necessary to significantly reduce the hypertension. As with the mechanisms by which increased adiposity (obesity) promote hypertension, the mechanisms by which CR reduce arterial pressure are not established. The relevant data suggest that a multitude of mechanisms may contribute simultaneously to reduce arterial pressure including improvements in nitric oxide (NO) and AMPK signaling, redox balance, renin-angiotensin system, and glucose tolerance. However, CR in animals does not consistently produce similar results with respect to improvements in arterial pressure. We have shown that perturbed dietary intake of nutrients (excessive cholesterol, glucose, and saturated fat) does not consistently exacerbate the MetS-associated hypertension while acute CR does not significantly reduce the hypertension despite improvements in other aspects of MetS. While partial recovery of the lost adiposity/body mass did not exacerbate the MetS-associated hypertension in OLETF rats, other detriments on cellular metabolism were identified suggesting that, at least during acute, metabolic perturbations, the mechanisms regulating arterial pressure are resistant to these cellular mechanisms. The complexity of the metabolic syndrome presents many challenges to the ability to dissect the mechanisms by which MetS risk factors promote the associated hypertension. Conversely, dissecting the mechanism by which CR ameliorates the MetS-associated hypertension remains equally challenging. Nonetheless, much more research on the mechanisms by which CR improves the MetS-associated hypertension is needed to gain a better understanding of the complex relationships among diet, hypertension, and MetS-related risk factors.