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Hypertension is a common, modifiable risk factor of cardiovascular mortality. At present, 30% to 40% of adults in developed countries suffer from hypertension.1 When hypertension was first recognized, control was difficult due to limited treatment options and often regarded as a fruitless endeavor. In 1931, Dr. Paul Dudley White wrote, “Hypertension may be an important compensatory mechanism which should not be tampered with, even were it certain that we could control it.”2 Starting in the 1930s, surgical sympathectomy to reduce sympathetic tone was observed to significantly lower blood pressure at the expense of significant procedural morbidity and long-term disability. It was not until the late 1960s that pharmacotherapy for hypertension became available and widespread. Pharmacologic treatment for hypertension has proven generally effective, spurred development of many classes of medications, and assisted in the reduction in mortality from cardiovascular disease. Despite this success, many patients have hypertension that remains uncontrolled. Many cases of uncontrolled hypertension may be attributed to inaction or lack of awareness on the part of patient or provider, but the prevalence of true treatment-resistant hypertension is increasing. In recent years, interest in modifying the sympathetic nervous system has reemerged with the advent of novel minimally invasive methods such as catheter-based renal artery denervation that can potentially restore more balanced autonomic nervous system physiology and offer alternative treatment options for systemic conditions such as hypertension. In this chapter, we will review what is known about the efficacy of catheter-directed autonomic modulation as a novel treatment of hypertension, discuss best practices to achieve desired results, and outline what the future may hold for this controversial area of endovascular medicine.



Although the pathophysiology of hypertension is complex and incompletely characterized, the sympathetic nervous system is known to play an important role. In essential hypertension, prior studies have demonstrated increased systemic sympathetic nerve firing as well as excessive sympathetic drive to the kidneys. In the 1850s, French physiologist Claude Bernard discovered that disrupting innervation of the greater splanchnic nerve resulted in diuresis and that electrical stimulation resulted in antidiuresis.3 Early work on the pressor nerves built the foundation for describing the sympathetic nervous system’s effect on regulation of blood pressure. In animal studies, stimulation of chemosensitive renal afferent nerves has been shown to increase systemic efferent sympathetic nerve activity and increase blood pressure.4 Renal efferent nerves increase systemic blood pressure by stimulating renin production, tubular reabsorption of sodium, and renal arterial vasoconstriction.5 Furthermore, dense sympathetic innervation of the renal tubules helps regulate pressure natriuresis and sodium excretion in the setting of hypertension, although this process is impaired in long-standing hypertension.

Direct measurement of renal sympathetic activation by sampling renal norepinephrine spillover confirms increased sympathetic drive to the kidneys in the setting of long-standing hypertension. Norepinephrine spillover is defined as the amount of norepinephrine escaping neuronal uptake and local metabolism and ...

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