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To the Editor: The renal sympathetic nerves have been identified as a major contributor to the complex pathophysiology of hypertension in both experimental models and in humans.¹ Patients with essential hypertension generally have increased efferent sympathetic drive to the kidneys, as evidenced by elevated rates of renal norepinephrine spillover, defined as the amount of transmitter that escapes neuronal uptake and local metabolism and thus “spills over” into the circulation. Hypertension is also characterized by an increased rate of sympathetic-nerve firing, possibly modulated by afferent signaling from renal sensory nerves.²–⁴

A 59-year-old male patient with long-standing essential hypertension that was . . .