What will increased sympathetic activity do

Deckert P. Heindl S. Struck J. Perras B. Dodt C. Evidence for lower sympathetic nerve activity in young adults with low birth weight J. Schobel H. Heusser K. Schmieder R. Veelken R. Fischer T. Luft F. Evidence against elevated sympathetic vasoconstrictor activity in borderline hypertension J. Sherwood A. Hinderliter A. Light K. Physiological determinants of hyperreactivity to stress in borderline hypertension Hypertension 25 Hornfeldt B. Arterial baroreceptor denervation impairs long-term regulation of arterial pressure during dietary salt loading Am.

Sawin L. Effect of arterial baroreceptor denervation on sodium balance Hypertension 40 Wang D. Lookingland K. Degeneration of capsaicin-sensitive sensory nerves leads to increased salt sensitivity through enhancement of sympathoexcitatory response Hypertension 37 Zhao Y. Increased salt sensitivity induced by impairment of sensory nerves: is nephropathy the cause?

Influence of arterial baroreceptors and intracerebroventricular guanabenz on synchronized renal nerve activity Acta Physiol. Functional significance of the pattern of renal sympathetic nerve activation Am. Rapp J. Dissecting the primary causes of genetic hypertension in rats Hypertension 18 I18 I Cardiopulmonary baroreflex in NaCl-induced hypertension in bordeline hypertensive rats Hypertension 29 Jones S. Renal mechanoreceptor dysfunction: an intermediate phenotype in spontaneously hypertensive rats Hypertension 33 Tank J.

Diedrich A. Genetic influences on baroreflex function in normal twins Hypertension 37 France C. Decreased pain perception and risk for hypertension: considering a common physiological mechanism Psychophysiology 36 Ohlsson W. Renal sympathetic neural mechanisms as intermediate phenotype in spontaneously hypertensive rats Hypertension 27 Johnson R. Gordon K. Suga S. Duijvestijn A. Griffin K. Renal injury and salt-sensitive hypertension after exposure to catecholamines Hypertension 34 Dominiak P.

Mann J. Glomerular hyperfiltration during sympathetic nervous system activation in early essential hypertension J. Castellani S. Ungar A. Cantini C. Impaired renal adaptation to stress in the elderly with isolated systolic hypertension Hypertension 34 Schneider M. Klingbeil A. Schlaich M. Langenfeld M. Impaired sodium excretion during mental stress in mild essential hypertension Hypertension 37 Oparil S. Sripairojthikoon W. Neuronal control of the kidney: contribution to hypertension Can.

Buranakarl C. Benjanirut C. Pondeenana S. Bovee K. Norepinephrine kinetics in dogs with experimentally induced renal vascular hypertension Am. Miyajima E. Yamada Y. Yoshida Y. Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism Hypertension 17 Elam M. Increased sympathetic nerve activity in renovascular hypertension Circulation 99 Gao S.

Jensen G. Reduced spontaneous baroreceptor sensitivity in patients with renovascular hypertension J. Head G. Burke S. Renal and cardiac sympathetic baroreflexes in hypertensive rabbits Clin.

Wiecek A. Heidland A. Gilge U. Kokot F. Kuczera M. Kiersztejn M. Enhanced activity of sympathetic renal nerves in hypertensive patients with unilateral renal ischemia—its relationship to plasma renin activity in renal venous blood Clin. Abboud F. Chapleau M. A novel effect of angiotensin on renal sympathetic nerve activity in mice J. Dendorfer A. Thornagel A. Raasch W. Tempel K. Angiotensin II induces catecholamine release by direct ganglionic excitation Hypertension 40 Cicha M.

Smith L. Impaired responsiveness of renal mechanosensory nerves in heart failure: role of endogenous angiotensin Am. Niederberger M. Aubert J. Nussberger J. Brunner H.

Waeber B. Sympathetic nerve activity in conscious renal hypertensive rats treated with an angiotensin converting enzyme inhibitor or an angiotensin II antagonist J. Differentiated response of the sympathetic nervous system to angiotensin-converting enzyme inhibition in hypertension Hypertension 36 Campese V.

Kogosov E. Renal afferent denervation prevents hypertension in rats with chronic renal failure Hypertension 25 Zhong H. Duong V. Losartan reduces central and peripheral sympathetic nerve activity in a rat model of neurogenic hypertension Hypertension 39 Zhang W. Hosaka M. Cyclosporine A-induced hypertension involves synapsin in renal sensory nerve endings Proc.

Elzinga L. Rosen S. Burdmann E. Hatton D. Lindsley J. Bennett W. The role of renal sympathetic nerves in experimental chronic cyclosporine nephropathy Transplantation 69 Tuncel M. Toto R. Victor R. Sympathetic overactivity as a cause of hypertension in chronic renal failure J. Hausberg M. Kosch M. Harmelink P. Sympathetic nerve activity in end-stage renal disease Circulation Zoccali C.

Mallamaci F. Tripepi G. Neuropeptide Y, left ventricular mass and function in patients with end stage renal disease J. Cowley A. Genomics and homeostasis Am. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search.

Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Quantification of renal sympathetic nerve activity. Primary or essential hypertension. Renovascular hypertension and angiotensin II. End-stage renal disease. Interactions between the sympathetic nervous system and the kidneys in arterial hypertension.

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Abstract Elevated sympathetic activity changes renal function and accelerates the development of hypertension. Arterial hypertension , Kidney , Sympathetic nervous system. Open in new tab Download slide. Long-term arterial pressure control: an analysis from animal experiments and computer and graphic models. Google Scholar PubMed. Google Scholar Crossref. Search ADS. Increased sympathetic nervous system activity and its therapeutic reduction in arterial hypertension, portal hypertension and heart failure.

Sympathetic nerve activity and neurotransmitter release in humans: translation from pathophysiology into clinical practice. Beta adrenergic control of macromolecule synthesis in neonatal rat heart, kidney and lung: relationship to sympathetic neuronal development.

Neurotrophin 3 rescues neuronal precursors from apoptosis and promotes neuronal differentiation in the embryonic metanephric kidney. Glial-cell-line-derived neurotrophic factor is required for bud initiation from ureteric epithelium.

Developing renal innervation in the spontaneously hypertensive rat: evidence for a role of the sympathetic nervous system in renal damage. Nerve growth factor mRNA content parallels altered sympathetic innervation in the spontaneously hypertensive rat.

Nerve growth factor gene and hypertension in spontaneously hypertensive rats. Nerve growth factor gene locus explains elevated renal nerve growth factor mRNA in young spontaneously hypertensive rats. Effects of neonatal central and peripheral catecholaminergic lesions on cardiac and renal nucleic acids and proteins.

Nephron number, renal function, and arterial pressure in aged GDNF heterozygous mice. Hypernoradrenergic innervation: its relationship to functional and hyperplastic changes in the vasculature of the spontaneously hypertensive rat. Noradrenergic content and turnover rate in kidney and heart shows gender and strain differences. Sympathetic activation in adipose tissue and skeletal muscle of hypertensive rats. Sympathetic-adrenal medullary response to stress in hyperactive and hypertensive rats.

Elevated sympathetic activity contributes to hypertension and salt sensitivity in diabetic obese Zucker rats. Phenotypic evidence of faulty neuronal norepinephrine reuptake in essential hypertension. Dissociation between muscle and skin sympathetic nerve activity in essential hypertension, obesity, and congestive heart failure.

Baroreflex control of sympathetic nerve activity in essential and secondary hypertension. Single-unit sympathetic discharge: quantitative assessment in human hypertensive disease. Differential arterial baroreflex regulation of renal, lumbar, and adrenal sympathetic nerve activity in the rat. Regional norepinephrine spillover in response to angiotensin-converting enzyme inhibition in healthy subjects. Renal sympathetic nerve responses to tempol in spontaneously hypertensive rats.

Basal sympathetic nerve activity is enhanced with augmentation of baroreceptor reflex in Wistar fatty rats: a model of obesity-induced NIDDM.

Hemodynamic characterization of hypertension induced by chronic intrarenal or intravenous infusion of norepinephrine in conscious rats. Chronic renal neuroadrenergic hypertension is associated with increased renal norepinephrine sensitivity and volume contraction.

Hypertension induced by chronic renal adrenergic stimulation is angiotensin dependent. Brief angiotensin converting enzyme inhibitor treatment in young spontaneously hypertensive rats reduces blood pressure long-term.

Persistent lowering of arterial pressure after continuous and intermittent therapy. Kidney-specific chromosome transfer in genetic hypertension: the Dahl hypothesis revisited. Long-term arterial pressure in spontaneously hypertensive rats is set by the kidney. The development of post-transplantation hypertension in recipients of an SHR kidney is independent of reinnervation of the graft.

Sympathetic activity in early renal post-transplantation hypertension in rats. Evidence for lower sympathetic nerve activity in young adults with low birth weight. Evidence against elevated sympathetic vasoconstrictor activity in borderline hypertension. Physiological determinants of hyperreactivity to stress in borderline hypertension. Arterial baroreceptor denervation impairs long-term regulation of arterial pressure during dietary salt loading. Through their inhibition of sympathetic nervous activity, I 1 binding agents carry the potential for specifically conferring cardiovascular protection in patients with hypertension.

In this review, the sympathetic neural pathophysiology of essential hypertension is catalogued, and the justification for the use of central sympathetic inhibition by I 1 binding agents such as rilmenidine in its treatment is presented. Measurement of the excretion of the sympathetic nervous neurotransmitter norepinephrine in urine is now largely obsolete as a test of human sympathetic nervous activity, whereas assay of the plasma concentration of norepinephrine, still widely used, has two major limitations.

The first is that no information is provided on regional sympathetic nervous function; sympathetic nervous system responses typically show regional differentiation that can be detected in clinical research only by techniques that assess organ-specific sympathetic function.

Clinical measurements of rates of sympathetic nerve firing and of norepinephrine release to plasma provide the most secure basis for studying regional sympathetic nervous function in patients with hypertension Figure 1. This technique provides a method for studying nerve firing rates, in subcutaneous sympathetic nerves distributed to skin and skeletal muscle Figure 1. The technique involves the insertion of fine tungsten electrodes through the skin, with positioning of the electrode tip in sympathetic fibers of, most commonly, the common peroneal or median nerves.

Multifiber recordings of bursts of nerve activity, synchronous with the heart beat, are generated. Neurotransmitter release can be studied clinically using radiotracer-derived measurements of the appearance rate of norepinephrine in plasma from individual organs 6 Figure 1. Microneurographic methods do not give access to sympathetic nerves of internal organs, a limitation that is overcome by using regional norepinephrine spillover measurements.

With infusion of tritiated norepinephrine and regional blood sampling from the coronary sinus and renal veins, neurotransmitter release from the heart and kidneys can be measured.

Heart rate power spectral analysis techniques are commonly applied as an alternative, noninvasive method for studying sympathetic function in the heart. With this technique, mathematical partitioning allows identification of individual, superimposed rhythms producing cyclical variation in heart rate and arterial pressure. The autonomic nervous system provides the principal effector mechanism for heart rate variability. Although the low-frequency heart rate variability approximately 0. Evidence drawn from a number of sources, utilizing both electrophysiologic and neurochemical techniques, provides compelling evidence that overactivity of the sympathetic nervous system is commonly present in younger patients with essential hypertension Figure 1.

In borderline and established hypertension, nerve firing rates in postganglionic sympathetic fibers passing to skeletal muscle blood vessels are increased. There is also increased spillover of the sympathetic neurotransmitter norepinephrine from the heart and kidneys, providing evidence of stimulated sympathetic outflow to these organs.

There have been some misgivings that sympathetic nervous activation in hypertension might, perhaps, simply represent an alerting response in the laboratory, additionally contributed to by anxiety resulting from recent diagnostic labeling of patients as hypertensive.

In a mental stress response, epinephrine secretion is increased and the sympathetic outflow to skeletal muscle vasculature typically is unchanged or reduced, whereas that to skin is increased, and hepatomesenteric sympathetic tone is increased.

The specific causes of the increased sympathetic activity in essential hypertension remain largely unknown, although genetic influences are evident and behavioral and lifestyle factors appear to be involved.

The heritability of sympathetic overactivity in primary human hypertension has been little studied. The limited search undertaken so far for single gene abnormalities involving the sympathetic nervous system has been unsuccessful in patients with high blood pressure. Sympathetic nervous activity does appear to be heritable in healthy subjects with normal blood pressure. In monozygotic twins, 16 skeletal muscle sympathetic nerve firing rates were found to be almost identical in individual pairs, unlike in randomly paired groupings of unrelated subjects in whom a wide range of nerve firing rates was evident.

Continuing uncertainty exists concerning the role of stress in the sympathetic activation of hypertensive patients and in the pathogenesis of human hypertension in general. Though studies substantiating a role for experimental stress in causing hypertension in laboratory animals are interesting and important, it is another matter to demonstrate that essential hypertension is due to psychosocial conflict.

Clinical, epidemiologic, and laboratory research does, however, provide increasingly strong support for the notion that behavioral and psychologic factors are of importance in the pathogenesis of human hypertension. Although the concept that in some patients essential hypertension may arise by psychosomatic mechanisms is not entirely unproven, there is a substantial body of supporting experimental and clinical evidence.

Long-term neural effects of stress on renal function is a probable mediating mechanism in blood pressure elevation. Patients with primary hypertension are commonly overweight. Because positive energy balance initiates thermogenesis by stimulation of the sympathetic nervous system, the sympathetic activation seen in essential hypertension could perhaps represent an adaptive response to overeating, a hypothesis proposed by Landsberg.

Calorie restriction reduces both sympathetic activity and blood pressure. There is selective activation of the sympathetic nerves to the kidneys and skeletal muscle vasculature in normotensive human obesity, but suppression of the cardiac sympathetic outflow 27 Figure 2.

The possible importance of activation of the renal sympathetic outflow in the pathogenesis of obesity-related hypertension is illustrated in a recent study on dogs made obese by overfeeding, where renal denervation prevented the development of hypertension.

Increased renal sympathetic activity in obesity may be a necessary cause for the development of hypertension and predisposes to hypertension development , but apparently is not a sufficient cause.

The discriminating feature of the obese who develop hypertension is absence of the adaptive suppression of cardiac sympathetic outflow seen in the normotensive obese. An additional factor possibly contributing to sympathetic nervous overactivity in hypertensive patients is sedentary lifestyle.

Regularly performed physical exercise produces long-term lowering of blood pressure. This antihypertensive effect of exercise is associated with, and most probably caused by, inhibition of the sympathetic nervous system, 30 especially the sympathetic nerves of the kidneys. Although the specific causes of the increased sympathetic activity in essential hypertension remain uncertain, there is growing evidence of an underlying disturbance in CNS monoaminergic control of sympathetic outflow, which may perhaps be the common mediating mechanism of peripheral sympathetic activation with stress, obesity, and physical inactivity.

Catecholaminergic neurons, releasing norepinephrine are widely distributed in the brain, but are located in particular in the medulla and pons. Electrophysiologic and anatomical experiments carried out in animals provide evidence of a connection between pressor noradrenergic hypothalamic and brainstem centers and sympathetic preganglionic neurons in the thoracolumbal cord.

Brain norepinephrine turnover can be estimated clinically by measuring the overflow of norepinephrine and its lipophilic metabolites into the internal jugular veins. In hypertensive patients, norepinephrine spillover from the brain on average is higher than in healthy subjects, as is the overflow into the internal jugular veins of the lipophilic metabolites of norepinephrine, DHPG, and MHPG. Cerebral venous sinus scans indicate that the increased overflow of norepinephrine, DHPG, and MHPG in hypertensive patients is from subcortical brain regions only.

Whereas the sympathetic activation present in human hypertension no doubt contributes to the blood pressure elevation, it seems to have additional adverse consequences in hypertensive patients, which go beyond this. Neural vasoconstriction can have undesirable metabolic effects, in skeletal muscle impairing glucose delivery to muscle, causing insulin resistance, and hyperinsulinemia, 37 and, in liver, retarding postprandial clearing of lipids, contributing to hyperlipidemia.

Similarly, high sympathetic nervous activity in the heart of hypertensive patients may be deleterious. The importance of neural mechanisms in arrhythmogenesis is well established, with stimulation of the cardiac sympathetic outflow predisposing to ventricular tachycardia and ventricular fibrillation in a variety of experimental models of arrhythmia development.

Increased cardiac sympathetic nerve firing, as measured by cardiac norepinephrine spillover, has also been demonstrated to commonly underlie clinical ventricular tachyarrhythmias.

However, in hypertensive patients, the relative contributions of left ventricular hypertrophy—which promotes reentrant arrhythmias—increased cardiac sympathetic activity, and coronary atherosclerosis to the arrhythmia development to which these patients are prone are uncertain at this stage. A trophic effect of sympathetic activation in the human heart is probable in hypertensive patients, perhaps contributing to the development of left ventricular hypertrophy.

A growth-promoting effect of norepinephrine on cardiac myocytes has been demonstrated in vitro. Examples of the former are the reduction in sympathetic nerve firing with I 1 binding agents, and of the latter, the reflex sympathetic activation produced by some slow channel calcium influx blockers.

This issue has been brought into recent focus by claims, hotly contested, that vasoactive calcium channel blockers may be harmful, in rapid-release pharmaceutical formulations, and perhaps increase cardiac risk by stimulating sympathetic activity in the heart. Given that sympathetic activation in hypertensive patients is centrally mediated, and probably contributes to unwanted cardiac effects, might it be appropriate to specifically recommend drugs inhibiting the sympathetic nervous system outflow in patients with human hypertension in whom sympathetic nervous activation is present?

One aim of antihypertensive drug therapy has been to use drugs whose mechanism of action is closely linked to the underlying pathophysiology of human hypertension. The expectation is that this will lead to greater efficacy in reducing clinical cardiovascular complications of hypertension, with a lesser incidence of adverse drug effects.

Tailoring of antihypertensive therapy to pathophysiology, however well based logically, given our present state of knowledge cannot be the primary therapeutic principle in hypertension care. This point being made, the important and actively researched—but to date incompletely answered—question remains: of all antihypertensive drugs, do those inhibiting the sympathetic nervous system best reduce cardiovascular risk?

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