Excessive sympathetic drive is undoubtedly a major contributing factor to the pathophysiology of hypertension and heart failure. Much of the excessive sympathetic drive in these conditions is directed to the kidney, where it leads to inappropriate sodium retention, renin stimulation, and diminished renal function. Less well appreciated is the role the kidney itself plays in the generation of increased sympathetic activity by way of the renal somatic afferent nerves. The kidney therefore is both target and contributor to increased sympathetic activity in these conditions. Although some current pharmacotherapy indirectly targets this "sympathorenal axis," resistant hypertension remains a common problem, and the prognosis in heart failure remains poor, especially in more severe cases. It is now possible to directly target this axis via procedures, which directly interrupt renal sympathetic efferent and afferent signaling. Other procedures involving chronic carotid nerve stimulation may indirectly influence renal sympathetic tone and so improve renal sodium handling. These techniques have demonstrated early promise in hypertension and offer significant potential in heart failure as well. Should their early promise be borne out in controlled studies, the "sympathorenal axis" will have been proven to be a key element in the pathophysiology of these 2 very common, and dangerous, conditions.