I want to thank the awards committee of the Council of the International Society of Hypertension for bestowing on me this singular honor. I took the occasion of this award to find out a little more about Franz Volhard [1]. In a career that dominated clinical medicine in Germany for a period of almost 50 years, his work advanced our understanding of the role played by the kidneys and by the sympathetic nervous system in the pathogenesis of hypertension. He chaired several departments of internal medicine, including the important department at the University of Frankfurt until he was dismissed, in 1938, for aggressively opposing political appointments to department chairs by the Nazis. He was reinstated in 1945 and rebuilt the department until his death in 1950. I am honored to receive an award that recognizes his important contributions.

My own work has, for the past 35 years, involved the sympathetic nervous system. That work led, in 1986, to the development of an hypothesis to explain the important and well-recognized association of hypertension and obesity, an association that, until recently, remained obscure [2]. Briefly stated, this hypothesis may be summarized as follows: obesity, whether associated with dietary excess or some diminished capacity for thermogenesis (a low metabolic rate) results in insulin resistance; insulin resistance serves to stabilize body weight by limiting fat stored in adipose tissue as well as, via the sympathetic nervous system, driving thermogenic mechanisms to restore energy balance (Fig. 1). According to this formulation, insulin resistance in the obese is a mechanism evolved for limiting further weight gain. Like any compensatory mechanism, however, there is a price to pay. In this situation, that price is the hyperinsulinemia and sympathetic activation which, via effects on the blood vessels, the heart and the kidneys, exerts a pro-hypertensive effect that, in susceptible individuals, causes hypertension (Fig. 1). Viewed in this light, the hypertension that