The complex interaction between overweight, hypertension, and sympathetic overactivity.

There is ample evidence in the epidemiological and clinical literature that hypertension and overweight are closely and causally interrelated. Sympathetic nervous system (SNS) overactivity has been well documented in both hypertension and overweight, but it is not clear whether this is a coincidental finding or whether the association reflects a mechanistic role of SNS in these two interrelated clinical conditions. Whereas in this review we focus on the evidence for a primary role of SNS in the development of hypertension and overweight, it is clear that the process can be initiated from other starting points such as primary overeating or sleep apnea. After overweight evolves, hormones secreted by fat cells further accelerate SNS overactivity, weight gain, and blood pressure increase. The main thesis of this article is that regardless of where the process started, the same clinical picture of hypertension, overweight, and SNS overactivity will emerge. There is good evidence that in genetically prone individuals, prolonged SNS stimulation elicits a down regulation of beta-adrenergic receptors. This in turn decreases the ability to dissipate calories and diminishes the beta-adrenoceptor-mediated vasodilatation. We hypothesize that beta-adrenoceptor downregulation is the linchpin in the association of SNS with overweight and hypertension.