Neurohumoral Stimulation

Zucker, Irving H.; Patel, Kaushik P.; Schultz, Harold D.

doi:10.1016/j.hfc.2011.08.007

Cited by 100 publications

(121 citation statements)

References 125 publications

(135 reference statements)

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“…NEUROHUMORAL EXCITATION, INCLUDING activation of the sympathetic nervous system, is prevalent in chronic heart failure (HF) patients with systolic dysfunction (11,15,17,19,54). Sympathetic nerve activity (SNA), whether measured indirectly by plasma norepinephrine levels (11), norepinephrine spillover (15), or decreased heart rate (HR) variability (17) or directly by microneurographic recordings (19), is found to be elevated.…”

mentioning

confidence: 99%

Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure

Antunes‐Correa

Nobre

Groehs

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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CE. Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure. Am J Physiol Heart Circ Physiol 307: H1655-H1666, 2014. First published October 10, 2014 doi:10.1152/ajpheart.00136.2014.-Previous studies have demonstrated that muscle mechanoreflex and metaboreflex controls are altered in heart failure (HF), which seems to be due to changes in cyclooxygenase (COX) pathway and changes in receptors on afferent neurons, including transient receptor potential vanilloid type-1 (TRPV1) and cannabinoid receptor type-1 (CB1). The purpose of the present study was to test the hypotheses: 1) exercise training (ET) alters the muscle metaboreflex and mechanoreflex control of muscle sympathetic nerve activity (MSNA) in HF patients.2) The alteration in metaboreflex control is accompanied by increased expression of TRPV1 and CB1 receptors in skeletal muscle.3) The alteration in mechanoreflex control is accompanied by COX-2 pathway in skeletal muscle. Thirty-four consecutive HF patients with ejection fractions Ͻ40% were randomized to untrained (n ϭ 17; 54 Ϯ 2 yr) or exercise-trained (n ϭ 17; 56 Ϯ 2 yr) groups. MSNA was recorded by microneurography. Mechanoreceptors were activated by passive exercise and metaboreceptors by postexercise circulatory arrest (PECA). COX-2 pathway, TRPV1, and CB1 receptors were measured in muscle biopsies. Following ET, resting MSNA was decreased compared with untrained group. During PECA (metaboreflex), MSNA responses were increased, which was accompanied by the expression of TRPV1 and CB1 receptors. During passive exercise (mechanoreflex), MSNA responses were decreased, which was accompanied by decreased expression of COX-2, prostaglandin-E2 receptor-4, and thromboxane-A2 receptor and by decreased in muscle inflammation, as indicated by increased miRNA-146 levels and the stable NF-B/ IB-␣ ratio. In conclusion, ET alters muscle metaboreflex and mechanoreflex control of MSNA in HF patients. This alteration with ET is accompanied by alteration in TRPV1 and CB1 expression and COX-2 pathway and inflammation in skeletal muscle. heart failure; muscle sympathetic nervous system; metaboreflex; mechanoreflex; exercise training

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confidence: 99%

Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure

Antunes‐Correa

Nobre

Groehs

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Also, the reduction of the LF/HF ratio at weeks 6 and 8 can be stemmed from the saturation of sympathovagal modulation. Therefore, the results imply that the desensitization of sympathovagal modulation occurs at a period between 4 and 6 weeks post-MI, which may represent the transition period from the compensatory to the decompensatory phase in the progression of heart failure (Mann and Bristow, 2005;Triposkiadis et al, 2009;Zucker et al, 2012). Differences in the timing of changes in parameters in HR, SDANN, and the LF/HF ratio occur after MI.…”

Section: Discussionmentioning

confidence: 87%

“…Previous studies focused on distinguishing compensatory hypertrophy and decompensatory heart failure in animal models by different hallmarks at each state, such as the extent of LV systolic function in Dahl-salt sensitive rats (Inoko et al, 1994), LV dilation with or without increase in stroke volume in MI rats (Francis et al, 2001), and the differential roles of angiogenic and anti-angiogenic factors in the hearts of mice with aortic stenosis (Givvimani et al, 2010). Nevertheless, the timing of occurrence of this transition after MI is poorly understood (Zucker et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Time course of diurnal rhythm disturbances in autonomic function of rats with myocardial infarction

Lee¹,

Han²,

Yi³

et al. 2013

Autonomic Neuroscience

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“…Much of this remodeling is due to alterations in the balance of autonomic and humoral factors that result from overstimulation of sympathetic efferent pathways (32) and the renin-angiotensin system (RAS), both local and systemic (25,30), with a corresponding decrease in central parasympathetic drive (31). Increased sympathetic activity evokes elevated levels of norepinephrine (NE) release within the heart (7).…”

mentioning

confidence: 99%

Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus

Hardwick

Ryan

Powers

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg Ϫ1 ·day Ϫ1 ) on remodeling of the guinea pig intrinsic cardiac plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the cardiac plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT 1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig cardiac plexus following MI is mediated, in part, by activation of both AT 1 and AT2 receptors.

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Neurohumoral Stimulation

Cited by 100 publications

References 125 publications

Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure

Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure

Time course of diurnal rhythm disturbances in autonomic function of rats with myocardial infarction

Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus

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