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1 uld help to further explore the link between neurohumoral activation after myocardial infarction and
2                   One possible mechanism for neurohumoral activation after myocardial infarction may
3 nuate sympathetic overactivity by modulating neurohumoral activation and renal afferent signalling, c
4                                              Neurohumoral activation characterizes heart failure.
5 eurosecretory cells (MNCs) may contribute to neurohumoral activation during disease states is unknown
6  contributes to exacerbated MNC activity and neurohumoral activation during disease states is unknown
7                              We propose that neurohumoral activation early in the postinfarction peri
8                                              Neurohumoral activation follows a stepwise pattern, with
9 erapies that interrupt, or even reverse, the neurohumoral activation in heart failure hold the greate
10 s as an underlying mechanism contributing to neurohumoral activation in neurogenic hypertension.
11 eus of hypertensive rats that contributes to neurohumoral activation in this disease.
12 trophy induced by stresses such as aging and neurohumoral activation is an independent risk factor fo
13      However, the significance of this early neurohumoral activation is unclear.
14                Understanding this pattern of neurohumoral activation may aid in understanding the sig
15 el of reduced cardiac output that mimics the neurohumoral activation observed in congestive heart fai
16 lar Dysfunction (SOLVD) trial suggested that neurohumoral activation precedes the development of symp
17   The fundamental mechanisms underlying this neurohumoral activation remain unknown, however.
18            The hemodynamic abnormalities and neurohumoral activation that accompany congestive heart
19 ypothesize that biomarkers for inflammation, neurohumoral activation, and cardiac injury can predict
20 ncrease in serum biomarkers of inflammation, neurohumoral activation, and myocardial injury increased
21         Patients with the greatest amount of neurohumoral activation, as estimated by plasma norepine
22 t in atrial stretch, hemodynamic change, and neurohumoral activation, contributes partially to the at
23 ocardial energetic perturbations result from neurohumoral activation, increased adverse free fatty ac
24 triuretic peptide levels, renal dysfunction, neurohumoral activation, myocardial necrosis and fibrosi
25 pe I collagen levels, suggesting more severe neurohumoral activation, myocyte necrosis, and fibrosis.
26 ar hypertrophy but to possibly be related to neurohumoral activation.
27 CO3(-) secretion (DBS), a measure of mucosal neurohumoral activation.
28  such as insulin resistance, in part through neurohumoral activation.
29 urable effects on haemodynamic measurements, neurohumoral activity, and left-ventricular remodelling
30     We investigated the roles of 3 different neurohumoral agonists as possible i-NANC neurotransmitte
31                                        All 3 neurohumoral agonists produced relaxation (with no diffe
32                 In HF, high Na(+) intake and neurohumoral alterations disrupt GAG structure, leading
33 H because of its known modulation of diverse neurohumoral and behavioral responses.
34                                          Its neurohumoral and hemodynamic profiles suggest possible a
35                     Its molecular, cellular, neurohumoral, and hemodynamic pathophysiological mechani
36             We investigated the hemodynamic, neurohumoral, and myocardial blood flow responses to men
37                                     Although neurohumoral antagonism has successfully reduced heart f
38 mitigate aberrant metabolism include intense neurohumoral antagonism, limitation of diuretics, correc
39 ed and emerging pharmacotherapies target the neurohumoral axis and reduce extravascular compression,
40                  Moreover, activation of the neurohumoral axis is unlikely to completely explain the
41                    (Systematic Withdrawal of Neurohumoral Blocker Therapy in Optimally Responding CRT
42 d randomized among 4 groups (continuation of neurohumoral blocker therapy, n = 20; withdrawal of reni
43 to investigate the feasibility and safety of neurohumoral blocker withdrawal in patients with normali
44                                     However, neurohumoral blocker withdrawal was hampered by cardiac
45                             The necessity of neurohumoral blockers in patients with heart failure who
46                    However, re-initiation of neurohumoral blockers occurred in 17 subjects because of
47 the control group and in the groups in which neurohumoral blockers were discontinued.
48  exposure as well as the consequence of this neurohumoral burst on cardiac stem cells (CSCs) are unkn
49             Growth factor-mediated pathways, neurohumoral cascades, and matricellular proteins deposi
50 s associated with acute myocardial ischemia, neurohumoral changes, and genetic predisposition in the
51 ed experimental CHF based on hemodynamic and neurohumoral characteristics that closely mimic human di
52 complex network of several physiological and neurohumoral circuits.
53 e brain, resulting from a complex network of neurohumoral circuits.
54 ught of as a passive tissue that responds to neurohumoral control and inflammatory mediators.
55  these in the context of the ideas about the neurohumoral control of alimentary physiology that were
56 ology, all have diurnal rhythms, as does the neurohumoral control of cardiac and kidney function.
57 significant advances in our knowledge of the neurohumoral control of exocrine pancreatic secretion, e
58 ignaling may be important for development of neurohumoral control of intestinal motor reflexes.
59         In addition to new insights into the neurohumoral control of pancreatic secretion, these find
60 cle), and the relative absence of regulatory neurohumoral control of small vessel segments of the cir
61 s is their role in mechanical, chemical, and neurohumoral coupling processes that tune myofilament ac
62                     These findings highlight neurohumoral differences as key modulators of cardiac au
63 ynaptic functions contributes to exacerbated neurohumoral drive in prevalent cardiovascular disorders
64                         Chronically elevated neurohumoral drive, and particularly elevated adrenergic
65 ta-PVN dendrites and ultimately leads to the neurohumoral dysfunction driving hypertension.
66 ect of hemodynamic stress or is secondary to neurohumoral effects in response to hemodynamic overload
67 a key (although presently undefined) role in neurohumoral excitation in humans with heart failure.
68                                              Neurohumoral excitation is organ specific, affecting the
69               Moreover, other stress-related neurohumoral factors appear to counter the repressive ef
70           When stimulated by a wide array of neurohumoral factors or when faced with an increase in v
71 teraction of factors that are extrinsic (eg, neurohumoral factors) and intrinsic (eg, circadian clock
72                     During critical illness, neurohumoral factors, cytokines, endothelin, and atrial
73 e kinase strongly activated by integrins and neurohumoral factors.
74  of chronic oral ET-A receptor antagonism on neurohumoral function, renal hemodynamics, and sodium ex
75     These results, which demonstrate Ca(2+), neurohumoral, growth factor, cytokine, and developmental
76 and large outcomes trials of treatments with neurohumoral inhibition have documented reduced adverse
77  to HF with reduced EF, large trials testing neurohumoral inhibition in HFpEF failed to reach a posit
78 ulation (EFS) in the presence and absence of neurohumoral inhibitors (tin protoporphyrin IX [SnPP IX]
79                    In in vitro studies using neurohumoral inhibitors and tetrodotoxin and the use of
80 aemia reperfusion, myocardial infarction and neurohumoral injury, common causes of myocardial death a
81 eperfusion injury, myocardial infarction and neurohumoral injury, suggesting that pathological action
82  represents a neural substrate through which neurohumoral inputs are integrated within the forebrain
83 mmation, myocardial cell death pathways, and neurohumoral mechanisms, are addressed.
84 ddition to its modulation by reflex-mediated neurohumoral mechanisms, HR is also under the direct inf
85 sation in health and to explore the putative neurohumoral mechanisms.
86 EGP) and hepatic insulin sensitivity through neurohumoral mechanisms.
87 le organ response in the absence of systemic neurohumoral mechanisms.
88  secretion are reviewed, with an emphasis on neurohumoral mechanisms.
89 tivated through mechanosensitive pathways or neurohumoral mediators may play a critical role in fibro
90 ciated with alterations in potassium and the neurohumoral mediators of extrarenal potassium disposal
91 nical stress, cytokines, growth factors, and neurohumoral mediators stimulate fibroblast activation,
92 such altered membrane currents and a changed neurohumoral milieu creates a substrate that is highly s
93  2 diabetes mellitus alters the systemic and neurohumoral milieu, leading to changes in metabolism an
94 and implantable cardioverter-defibrillators; neurohumoral modification by baroreflex and vagal stimul
95                                      Diverse neurohumoral or mitochondrial stresses transiently induc
96 n contrast, CSCs were resistant to the acute neurohumoral overload.
97 ted to catecholamine stimulation to simulate neurohumoral overstimulation.
98 ents of Mozart's piano sonatas, we propose a neurohumoral pathway by which music might exert its seda
99 NaCl, regulate sympathetic drive and a novel neurohumoral pathway mediated by both brain and circulat
100 ither directly or through a leptin-regulated neurohumoral pathway.
101 d establish CaMKII as a nodal signal for the neurohumoral pathways associated with poor outcomes afte
102 iastolic function, deleterious activation of neurohumoral pathways, and high morbidity and mortality.
103                          The cardiorenal and neurohumoral properties of mANP compared with ANP were a
104 s modifying hemodynamics and cell biology by neurohumoral receptor blockade are evolving, exploring t
105 ypes expressed the same ion transporters and neurohumoral receptors, suggesting the importance of bal
106                      To circumvent potential neurohumoral reflexes, cardiac efficiency was additional
107  review highlights recent discoveries in the neurohumoral regulation of pancreatic exocrine secretion
108 e in the generation of a systemic, polymodal neurohumoral response to a hyperosmotic challenge.
109 ation in plasma osmolality elicits a complex neurohumoral response, including an activation of the sy
110 imilar to its role in the counter-regulatory neurohumoral responses to glucoprivation.
111 , including motor behaviours and homeostatic neurohumoral responses.
112 udy examined the role of angiotensin II as a neurohumoral signal for the myogenic tone in the interna
113        The adult heart responds to excessive neurohumoral signaling and workload by a pathological gr
114 s in active and passive membrane properties, neurohumoral signaling, and genetic determinants that pr
115  growth in response to pressure overload and neurohumoral signaling, whereas mice lacking HDAC5, a cl
116 d cellular mechanism that transforms diverse neurohumoral signals into a key behavioral output.
117 hormone angiotensin II (AngII) are two major neurohumoral signals that regulate body fluid homeostasi
118 luid homeostasis requires the integration of neurohumoral signals to coordinate behavior, neuroendocr
119 ctions of cell-specific regulatory pathways, neurohumoral signals, and changes in substrate availabil
120 were subjected to ischemic injury or chronic neurohumoral stimulation and monitored for survival, car
121 f activation of ANP synthesis despite marked neurohumoral stimulation by the growth promoters ET and
122 ontribution of mechanical load compared with neurohumoral stimulation in vivo with specific focus on
123 this situation that have the least effect on neurohumoral stimulation of the pancreas.
124 2 abolishes the positive inotropic effect of neurohumoral stimulation with ET-1 and protects from its
125                                      Despite neurohumoral stimulation, LV mass index and myocyte diam
126 is in response to ischemic injury or chronic neurohumoral stimulation.
127 rption in isolated crypts that are devoid of neurohumoral stimulation.
128 rt processes plus fluid secretion induced by neurohumoral stimulation.
129 uring hemodynamic stress, catecholamines and neurohumoral stimuli may induce co-activation of G(q)-co
130  adult rat ventricular myocytes treated with neurohumoral stimuli such as angiotensin II (Ang II) and
131 e that in adult cardiomyocytes two important neurohumoral stimuli that induce hypertrophy, endothelin
132 hermore, HDAC phosphorylation in response to neurohumoral stimuli that induce hypertrophy, such as en
133 nse to increased ventricular wall tension or neurohumoral stimuli, the myocardium undergoes an adapti
134 ar energy status, is activated by stress and neurohumoral stimuli.
135 y and heart failure, driven by mechanical or neurohumoral stress.
136 rophy is a common response to circulatory or neurohumoral stressors as a mechanism to augment contrac
137     Blood pressure is regulated by a complex neurohumoral system including the renin-angiotensin-aldo
138 with combined modulation of the ET and other neurohumoral systems in CHF are required.
139 econdary to vasodilatation and activation of neurohumoral systems.
140 econdary to vasodilatation and activation of neurohumoral systems.
141 econdary to vasodilatation and activation of neurohumoral systems.
142 proaches, such as antagonists to a number of neurohumoral targets (ie, endothelin [tezosentan], vasop
143 t to assess the primary preventive effect of neurohumoral therapy in high-risk diabetic patients sele
144 m (Na(+)) and fluid retention resulting from neurohumoral up-regulation.

 
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