Dissociation Between Muscle and Skin Sympathetic Nerve Activity in Essential Hypertension, Obesity, and Congestive Heart Failure

Colombo, M.; Seravalle, Gino; Spaziani, Domenico; Mancia, Giuseppe

doi:10.1161/01.hyp.31.1.64

Cited by 228 publications

(197 citation statements)

References 44 publications

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“…16,17 The fifth point, confirming previous findings of an increase in urinary or plasma NE values, 18,19 is that the same phenomenon can be observed not only in obese hypertensive but also in obese normotensive subjects. 20,21 Thus, sympathetic overactivity can be detected in hypertensive patients with different degrees of BP elevation and of different ages. The very initial hypertensive stages are by no means an exception, which suggests that this phenomenon may have a role in both the maintenance and the initiation of this condition.…”

Section: Evidence For Sympathetic Activationmentioning

confidence: 99%

“…Second, the sympathetic overactivity characterizing essential HT may not be generalized to the whole cardiovascular system, as exemplified by the evidence that both in mild and more severe essentialhypertensive patients, the number of sympathetic bursts is increased in fibers innervating skeletal muscle tissue but not in fibers innervating the skin. 21 This heterogeneous behavior (which is also typical of obesity and heart failure 21 ) may originate from the peculiarity of the mechanisms that govern skin vasomotor tone. This tone has been shown to exquisitely depend on autonomic modulation, in response, however, not from the baroreflex (as is muscle sympathetic tone 4,8 ) but from thermoregulatory centers located in the hypothalamus.…”

Section: Evidence For Sympathetic Activationmentioning

confidence: 99%

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Sympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage

et al. 1999

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Abstract-Although animal models of hypertension have clearly shown that high blood pressure is associated with and is probably caused by an increase in sympathetic cardiovascular influences, a similar demonstration in humans has been more difficult to obtain for methodological reasons. There is now evidence, however, of increased sympathetic activity in essential hypertension. This article will review this evidence by examining data showing that plasma norepinephrine is increased in essential hypertension and that this is also the case for systemic and regional norepinephrine spillover, as well as for the sympathetic nerve firing rate in the skeletal muscle nerve district. Evidence will also be provided that sympathetic activation is a peculiar feature of essential hypertension, particularly in its early stages, with secondary forms of high blood pressure not usually characterized by an increased central sympathetic outflow. Humoral, metabolic, reflex, and central mechanisms are likely to be the factors responsible for the adrenergic activation characterizing hypertension, which may also promote the development and progression of the cardiac and vascular alterations that lead to hypertension-related morbidity and mortality, independent of blood pressure values. This represents the rationale for considering sympathetic deactivation one of the major goals of antihypertensive treatment. Key Words: nervous system, sympathetic Ⅲ hypertension, essential Ⅲ hypertension, secondary Ⅲ pressoreceptors Ⅲ hypertrophy Ⅲ norepinephrine N eural adrenergic factors have long been hypothesized to be important in the initiation and maintenance of high blood pressure (BP). For a long time, however, the evidence supporting this hypothesis was largely limited to the results of studies performed in different animal models of hypertension (HT), in which an enhanced sympathetic drive to the heart and peripheral circulation was shown either to trigger a persistent BP elevation or to maintain the BP elevation originally induced by nonadrenergic mechanisms. [1][2][3][4] This picture has changed in the past 20 years or so because a variety of techniques that allow indirect or direct quantification of adrenergic cardiovascular influences have all provided evidence of an activation of the sympathetic nervous system (SNS) in human HT as well. This article will review the evidence that sympathetic activity is increased in essential HT and that this increase may have a pathogenetic role. It will also discuss 2 other issues, ie, (1) the mechanisms that lead to sympathetic hyperactivity in essential HT and (2) the role exerted by this hyperactivity in the progression of the cardiovascular alterations that may complicate the hypertensive state. Evidence for Sympathetic ActivationIn the past 30 years, several techniques designed to quantify sympathetic cardiovascular influences in humans have shown them to be increased in essential HT. More than 25 years ago, for example, Julius and coworkers 5 showed that the elevated resting heart rate values of bo...

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Section: Evidence For Sympathetic Activationmentioning

confidence: 99%

Section: Evidence For Sympathetic Activationmentioning

confidence: 99%

Sympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage

et al. 1999

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“…Approximately 40% of patients with untreated essential hypertension have chronically increased cardiac and renal spillover of norepinephrine and increased rates of efferent sympathetic nerve firing in the outflow to the skeletal muscle vasculature (27,33,34). These alterations are most evident in relatively young patients.…”

Section: Neurogenic Essential Hypertensionmentioning

confidence: 99%

“…Chronic sympathetic nervous activation contributes to hypertension by stimulating the heart and elevating cardiac output in the early phases; by neurally mediated vasoconstriction; and, in the kidney, by augmenting renin secretion and tubular reabsorption of sodium (27,33,34,36,37). The renal sympathetic activation may be of particular importance for the development of the hypertension.…”

Section: Neurogenic Essential Hypertensionmentioning

confidence: 99%

Dysautonomias: Clinical Disorders of the Autonomic Nervous System

Goldstein

Robertson²,

Esler³

et al. 2002

Ann Intern Med

175

111

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The term dysautonomia refers to a change in autonomic nervous system function that adversely affects health. The changes range from transient, occasional episodes of neurally mediated hypotension to progressive neurodegenerative diseases; from disorders in which altered autonomic function plays a primary pathophysiologic role to disorders in which it worsens an independent pathologic state; and from mechanistically straightforward to mysterious and controversial entities. In chronic autonomic failure (pure autonomic failure, multiple system atrophy, or autonomic failure in Parkinson disease), orthostatic hypotension reflects sympathetic neurocirculatory failure from sympathetic denervation or deranged reflexive regulation of sympathetic outflows. Chronic orthostatic intolerance associated with postural tachycardia can arise from cardiac sympathetic activation after "patchy" autonomic impairment or blood volume depletion or, as highlighted in this discussion, from a primary abnormality that augments delivery of the sympathetic neurotransmitter norepinephrine to its receptors in the heart. Increased sympathetic nerve traffic to the heart and kidneys seems to occur as essential hypertension develops. Acute panic can evoke coronary spasm that is associated with sympathoneural and adrenomedullary excitation. In congestive heart failure, compensatory cardiac sympathetic activation may chronically worsen myocardial function, which rationalizes treatment with ␤-adrenoceptor blockers. A high frequency of positive results on tilt-table testing has confirmed an association between the chronic fatigue syndrome and orthostatic intolerance; however, treatment with the salt-retaining steroid fludrocortisone, which is usually beneficial in primary chronic autonomic failure, does not seem to be beneficial in the chronic fatigue syndrome. Dysautonomias are an important subject in clinical neurocardiology. The notion that the sympathetic nervous system coordinates body functions probably originated with the second-century Greek physician Galen, who taught that nerves were hollow tubes distributing "animal spirits" in the body, thereby fostering concerted action, or "sympathy," of the organs. In 1552, Bartolomeo Eustachius first depicted the sympathetic nerves and the adrenal glands. Winslow reintroduced the sympathetic nervous system in 1732 to describe the chains of ganglia and nerves connected to the thoracic and lumbar spinal cord.The functions of these structures remained unknown until the 19th century, when Bernard and others first reported the effects of sympathetic nerve stimulation. In 1895, Oliver and Schäfer described the potent cardiovascular stimulatory effects of adrenal extracts. Soon afterward-almost exactly a century ago-Abel and Takamine identified epinephrine ("adrenaline" in British and European countries) as the active principle of the adrenal gland.Also in the late 19th century, Langley coined the term autonomic nervous system to denote the portion of the nervous system largely responsible for involuntary, unc...

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“…At present it is uncertain whether a similar linking of reduced NGF production to increased sympathetic nerve firing rates exists in essential hypertension which, as for heart failure, is often accompanied by sympathetic nervous activation. 18 In the Japanese spontaneously hypertensive rate, in which sympathetic stimulation is also well documented, perhaps surprisingly sympathetic hyperinnervation is present, driven by increased expression of NGF. 19 Definitive experiments in essential hypertension have not yet been reported.…”

mentioning

confidence: 99%