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Journal ArticleDOI

Sympathetic Nervous System and Hypertension

01 Mar 2013-Hypertension (Lippincott Williams & Wilkins)-Vol. 61, Iss: 3, pp 556-560
TL;DR: This review will encompass recent publications dealing with the sympathetic nervous system and hypertension, focusing on those recently published in Hypertension.
Abstract: With the development and implementation of device-based therapeutic interventions to decrease renal and systemic nerve activity in patients with resistant hypertension, there has been an increase in research dealing with the role of the sympathetic nervous system in hypertension. These interventions have produced substantial decreases in blood pressure in patients wherein pharmacological treatments, including agents which inhibit the effects of the renin–angiotensin–aldosterone system, have failed serves to confirm and reassert the essential role of the sympathetic nervous system in hypertension. This review will encompass recent publications dealing with the sympathetic nervous system and hypertension, focusing on those recently published in Hypertension . ### Obesity-Related Hypertension Although there has been a debate as to whether sympathetic activation is a cause or consequence of obesity, the studies noted below support the view that it is the obesity that leads to sympathetic activation. The importance of this sympathetic activation for the development of the hypertension is supported by the finding that renal denervation prevents the development of obesity hypertension in the dog. Studies have now focused on the developmental phase of obesity hypertension regarding the renal sympathoexcitation. In rabbits fed high-fat diets, body weight, plasma insulin and leptin concentrations, mean arterial pressure, heart rate, and renal sympathetic nerve activity were all increased after 1 week.1 Mean arterial pressure and body weight continued to increase over 3 weeks of high-fat diet, whereas heart rate and renal sympathetic nerve activity did not change further. Arterial baroreflex control of renal sympathetic nerve activity was attenuated from the first week of the high-fat diet. Excitatory responses to air jet stress diminished over 3 weeks of high-fat diet. Resumption of normal diet normalized glucose, insulin, leptin, and heart rate, but body weight, visceral fat content, mean arterial pressure, and renal sympathetic nerve activity remained elevated. Increased renal sympathetic nerve activity …

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Citations
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Journal ArticleDOI
TL;DR: With prolonged obesity and development of target organ injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation.
Abstract: Excess weight gain, especially when associated with increased visceral adiposity, is a major cause of hypertension, accounting for 65% to 75% of the risk for human primary (essential) hypertension. Increased renal tubular sodium reabsorption impairs pressure natriuresis and plays an important role in initiating obesity hypertension. The mediators of abnormal kidney function and increased blood pressure during development of obesity hypertension include (1) physical compression of the kidneys by fat in and around the kidneys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased sympathetic nervous system activity. Activation of the renin-angiotensin-aldosterone system is likely due, in part, to renal compression, as well as sympathetic nervous system activation. However, obesity also causes mineralocorticoid receptor activation independent of aldosterone or angiotensin II. The mechanisms for sympathetic nervous system activation in obesity have not been fully elucidated but may require leptin and activation of the brain melanocortin system. With prolonged obesity and development of target organ injury, especially renal injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation. Unless effective antiobesity drugs are developed, the effect of obesity on hypertension and related cardiovascular, renal and metabolic disorders is likely to become even more important in the future as the prevalence of obesity continues to increase.

782 citations


Cites background from "Sympathetic Nervous System and Hype..."

  • ...ute to generalized sympathoinhibition and BP reduction after RDN.(70,71) However, reductions in BP after RDN do not seem...

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  • ...various forms of experimental hypertension, including renovascular hypertension.(70) However, the role of renal afferents in hypertension has been controversial....

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  • ...30 mm Hg systolic BP and 10 to 12 mm Hg diastolic BP for ≤24 months.(70,71) When 24-hour ambulatory BP was measured...

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  • ...Early investigators, including Harry Goldblatt74 who first developed reproducible models of renovascular hypertension, found no evidence that renal or splanchnic nerves are necessary for development or maintenance of renovascular hypertension.75 The concept that renal afferents contribute to the BP lowering effects of RDN initially derived from a report that wholebody norepinephrine spillover and MSNA were reduced 1 year after RDN in a single patient.76 Further support for this concept came from the observation that in obese patients with resistant hypertension, radiofrequency RDN decreased MSNA (by only 12% to 14%), as well as BP for ≤1 year.71,77 These findings were interpreted as evidence that interrupting afferent renal nerve pathways to the brain may contribute to generalized sympathoinhibition and BP reduction after RDN.70,71 However, reductions in BP after RDN do not seem to be correlated with reductions in MSNA and some investigators have failed to observe long-term reductions in MSNA after RDN.78 Thus, it is still uncertain whether RDN causes significant decreases in SNA to other organs besides the kidneys....

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Patent
05 Oct 2005
TL;DR: In this article, a pulsed electric field was used to induce electroporation or electrofusion of percutaneous intravascular vessels to reduce expansion of an acute myocardial infarction, reduce or prevent the onset of morphological changes that are affiliated with congestive heart failure, and/or be efficacious in the treatment of end stage renal disease.
Abstract: Methods and apparatus are provided for renal neuromodulation using a pulsed electric field to effectuate electroporation or electrofusion. It is expected that renal neuromodulation (e.g., denervation) may, among other things, reduce expansion of an acute myocardial infarction, reduce or prevent the onset of morphological changes that are affiliated with congestive heart failure, and/or be efficacious in the treatment of end stage renal disease. Embodiments of the present invention are configured for percutaneous intravascular delivery of pulsed electric fields to achieve such neuromodulation.

751 citations

Patent
03 Jun 2005
TL;DR: A method and apparatus for treatment of heart failure, hypertension and renal failure by stimulating the renal nerve is described in this paper, where the goal is to reduce the sympathetic activity of renal nerve.
Abstract: A method and apparatus for treatment of heart failure, hypertension and renal failure by stimulating the renal nerve. The goal of therapy is to reduce sympathetic activity of the renal nerve. Therapy is accomplished by at least partially blocking the nerve with drug infusion or electrostimulation. Apparatus can be permanently implanted or catheter based.

626 citations

Patent
14 Aug 2006
TL;DR: In this article, thermally-induced renal neuromodulation is achieved via delivery of a pulsed thermal therapy, where the parameters of the neural fibers, of non-target tissue, or of the thermal energy delivery element, may be monitored via one or more sensors.
Abstract: Methods and apparatus are provided for thermally-induced renal neuromodulation. Thermally-induced renal neuromodulation may be achieved via direct and/or via indirect application of thermal energy to heat or cool neural fibers that contribute to renal function, or of vascular structures that feed or perfuse the neural fibers. In some embodiments, parameters of the neural fibers, of non-target tissue, or of the thermal energy delivery element, may be monitored via one or more sensors for controlling the thermally-induced neuromodulation. In some embodiments, protective elements may be provided to reduce a degree of thermal damage induced in the non-target tissues. In some embodiments, thermally-induced renal neuromodulation is achieved via delivery of a pulsed thermal therapy.

488 citations

Patent
14 Nov 2007
TL;DR: In this article, a non-continuous circumferential treatment of a body lumen is described, where an apparatus is used to deliver energy at a first lengthwise and angular position within the lumen to create a less-than-full treatment zone at the first position.
Abstract: Methods and apparatus are provided for non-continuous circumferential treatment of a body lumen. Apparatus may be positioned within a body lumen of a patient and may deliver energy at a first lengthwise and angular position to create a less-than-full circumferential treatment zone at the first position. The apparatus also may deliver energy at one or more additional lengthwise and angular positions within the body lumen to create less-than-full circumferential treatment zone(s) at the one or more additional positions that are offset lengthwise and angularly from the first treatment zone. Superimposition of the first treatment zone and the one or more additional treatment zones defines a non-continuous circumferential treatment zone without formation of a continuous circumferential lesion. Various embodiments of methods and apparatus for achieving such non-continuous circumferential treatment are provided.

424 citations

References
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Journal ArticleDOI
TL;DR: Catheter-based renal denervation can safely be used to substantially reduce blood pressure in treatment-resistant hypertensive patients and should be continued, according to the authors.

2,200 citations

Journal ArticleDOI
TL;DR: In this article, a proof-of-principle trial of therapeutic renal sympathetic denervation in patients with resistant hypertension (i.e., systolic blood pressure ≥160 mm/hg on three or more antihypertensive medications, including a diuretic) was conducted to assess safety and blood-pressure reduction effectiveness.

1,985 citations

Book
01 Jul 2011
TL;DR: The renal nerve is the communication link between the central nervous system and the kidney as discussed by the authors, which is the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated.
Abstract: The renal nerves are the communication link between the central nervous system and the kidney. In response to multiple peripheral and central inputs, efferent renal sympathetic nerve activity is altered so as to convey information to the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated. At the level of each of these individual components, information transfer occurs via interaction of the neurotransmitter released at the sympathetic nerve terminal-neuroeffector junction with specific postjunctional receptors coupled to defined intracellular signaling and effector systems. In response to normal physiological stimuli, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. Afferent input from sensory receptors located in the kidney participates in this reflex control system via renorenal reflexes that enable total renal function to be self-regulated and balanced between the two kidneys. In pathophysiological conditions, abnormal regulation of efferent renal sympathetic nerve activity contributes significantly to the associated abnormalities of renal function which, in turn, are of importance in the pathogenesis of the disease.

1,288 citations

Journal Article
TL;DR: Catheter-based renal denervation causes substantial and sustained blood-pressure reduction, without serious adverse events, in patients with resistant hypertension, in a proof-of-principle trial of therapeutic renal sympathetic denervation.

1,284 citations

Journal ArticleDOI
TL;DR: The renal sympathetic nerves have been identified as a major contributor to the complex pathophysiology of hypertension in both experimental models and in humans and may be modulated by afferent signaling from renal sensory nerves.
Abstract: 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 . . .

864 citations

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