Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang, Wei; Chen, Jwo Sheng; Zucker, Irving H.

doi:10.1161/01.cir.81.6.1959

Cited by 136 publications

(72 citation statements)

References 26 publications

(17 reference statements)

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“…[3][4][5][6][12][13][14][15][16] These uniform findings of sympathetic activation directed to tissues governed by the baroreflexes have prompted the concept that impaired baroreflex restraint underlies sympathetic activation. It is unknown if increased sympathetic neural outflow in heart failure is limited to regions governed by the baroreflexes or is generalized to all tissues -a distinction with mechanistic implications.…”

Section: Methods and Resultsmentioning

confidence: 99%

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

et al. 1994

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BACKGROUND Sympathetic excitation characterizes heart failure, but the underlying mechanisms remain unknown. Abnormal baroreflex restraint of sympathetic neural outflow has been proposed, since baroreflexes are known to be abnormal in heart failure. The purpose of this study was to determine if sympathetic activation in humans with heart failure is limited to regions governed by the baroreflexes or is generalized to other regions free from baroreflex control. METHODS AND RESULTS We report the first direct recordings of skin sympathetic nerve activity (free from baroreflex control) in humans with heart failure and compare simultaneous skin and muscle (baroreflex-dependent) sympathetic peroneal nerve activity in six patients with severe heart failure (mean left ventricular ejection fraction, 0.19 +/- 0.06) and in six age-matched normal control subjects. Although muscle sympathetic nerve activity was markedly increased in heart failure patients (heart failure versus controls, 69 +/- 3 versus 21 +/- 2 bursts per minute; P < .001), skin sympathetic nerve activity was not increased (heart failure versus controls, 12 +/- 1 versus 15 +/- 1 bursts per minute; P = NS). CONCLUSIONS The finding that skin sympathetic nerve activity in contrast to muscle sympathetic nerve activity is not increased in heart failure supports the concept that an altered reflex system, such as the baroreflexes, with nonuniform effects on muscle and skin sympathetic nerve activity, underlies sympatho-excitation in heart failure.

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Section: Methods and Resultsmentioning

confidence: 99%

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

et al. 1994

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“…1,2 This abnormality increases cardiovascular risk. 3 Recent studies indicate that the blunted arterial baroreflex is related to an enhanced central angiotensin II (Ang II) mechanism, because blockade of Ang II type 1 receptors (AT 1 Rs) in the brain restored baroreflex sensitivity.…”

mentioning

confidence: 99%

Exercise Training Prevents Arterial Baroreflex Dysfunction in Rats Treated With Central Angiotensin II

et al. 2007

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Abstract-Angiotensin II (Ang II)-induced arterial baroreflex dysfunction is associated with superoxide generation in the brain. Exercise training (EX) improves baroreflex function and decreases oxidative stress in cardiovascular diseases linked to elevated central Ang II. The aim of this study was to determine whether previous EX prevents baroreflex impairment caused by central administration of exogenous Ang II via an Ang II-superoxide mechanism. Four groups of rats were used: non-EX artificial cerebrospinal fluid infused, non-EX Ang II infused, EX artificial cerebrospinal fluid infused, and EX Ang II infused. Rats were treadmill trained for 3 to 4 weeks and subjected to intracerebroventricular infusion of Ang II over the last 3 days of EX. Twenty-four hours after the end of EX, the arterial baroreflex was assessed in anesthetized rats. Key Words: exercise Ⅲ baroreflex Ⅲ sympathetic nerve activity Ⅲ reactive oxygen species Ⅲ AT 1 receptor I mpairment of arterial baroreflex function is an important feature in cardiovascular diseases, such as chronic heart failure (CHF) and hypertension. 1,2 This abnormality increases cardiovascular risk. 3 Recent studies indicate that the blunted arterial baroreflex is related to an enhanced central angiotensin II (Ang II) mechanism, because blockade of Ang II type 1 receptors (AT 1 Rs) in the brain restored baroreflex sensitivity. 4 Intracerebroventricular (icv) infusion of Ang II depresses arterial baroreflex function in normal animals. 5 However, specific brain nuclei and the intracellular mechanism for Ang II-induced baroreflex dysfunction have not been fully identified. The paraventricular nucleus (PVN) of the hypothalamus plays an important role in the control of baroreflex function and sympathetic drive. 6 Furthermore, the PVN contains a high density of AT 1 R 7 and is a candidate region to respond to Ang II in the cerebrospinal fluid. 8 Several lines of evidence show that reduced nicotinamideadenine dinucleotide phosphate (NAD[P]H) oxidase-derived reactive oxygen species (ROS) are novel mediators of Ang II signaling in the central nervous system. 9 Pretreatment with adenoviral-mediated superoxide dismutase prevents Ang IIinduced hypertension and the increased superoxide production. 10 On the other hand, the AT 1 R antagonist losartan abolishes Ang II-stimulated superoxide generation. 9 Increases in superoxide production may contribute to impaired arterial baroreflex function. 5,11 Conversely, antioxidant treatment improves baroreflex sensitivity. 11 Exercise training (EX) has been demonstrated to alter neural control of the circulation, including influencing arterial baroreflex function. 12 Although the effects of EX on baroreflex function in normal subjects and animals are increased, 12 decreased, 13,14 or unchanged, 15 EX consistently increases baroreflex sensitivity in CHF and hypertensive subjects. 16 -18 The mechanisms responsible for the training-induced improvement of baroreflex function involve changes in central and peripheral components of the baroreflex arc....

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“…12 In the study by Wang et al, 1 exposure of the isolated carotid sinus to ouabain in the presence of aldosterone did not restore baroreceptor activity. Thus, the inhibitory influence of aldosterone on baroreceptor activity does not appear to involve increased Na + ,K + -ATPase activity and consequently does not fully account for the decreased baroreceptor sensitivity observed in heart failure.…”

Section: Future Directions For Researchmentioning

confidence: 93%

Are arterial pressure and deformation the sole determinants of baroreceptor activity? Importance of humoral and endothelial modulation in normal and disease states.

Chapleau¹

1992

Hypertension

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A rterial baroreceptors located in the carotid si-/ \ nuses and aortic arch play a major role in A. \ -control of circulation and regulation of arterial pressure. Increased arterial pressure triggers increased frequency of baroreceptor discharge, which leads to reflex adjustments that buffer the rise in pressure. It is established that baroreceptors are not activated by increases in arterial pressure directly but instead are activated by the increased vascular stretch or strain that accompanies the rise in pressure. Mechanical deformation of the baroreceptor nerve endings is usually considered the primary or even the sole determinant of the frequency of baroreceptor discharge. Are there other factors besides deformation that are important in activation of baroreceptors?In this issue of Hypertension, Wang et al 1 report that exposure of the vascularly isolated carotid sinus in anesthetized dogs to the hormone aldosterone suppresses activation of baroreceptors without a change in vascular stretch as measured with sonomicrometer crystals. What is the mechanism of aldosterone-induced suppression of baroreceptor activity? Wang et al 1 demonstrate that the inhibitory effect of aldosterone is dependent on the presence of intact endothelium and is blocked by the aldosterone receptor antagonist spironolactone. The simplest scenario is that aldosterone binds to its receptor in endothelial cells and alters the release of a diffusable mediator that acts directly on baroreceptor neurons to modulate their sensitivity. This study is the first to show that aldosterone modulates baroreceptor activity and adds to the growing evidence that humoral and endothelial factors modulate to a significant extent the sensitivity of baroreceptors. Evidence for Humoral/Endothelial Modulationof Baroreceptor Activity Numerous studies dating back as far as the 1950s have demonstrated that various neurohumoral factors act locally in the carotid sinuses and aortic arch to modulate baroreceptor activity. 2 The majority of these studies,

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Carotid sinus baroreceptor sensitivity in experimental heart failure.

Cited by 136 publications

References 26 publications

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

Exercise Training Prevents Arterial Baroreflex Dysfunction in Rats Treated With Central Angiotensin II

Are arterial pressure and deformation the sole determinants of baroreceptor activity? Importance of humoral and endothelial modulation in normal and disease states.

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