ライフサイエンスコーパス: neurohumoral

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 Neurohumoral activation characterizes heart failure.

4 eurosecretory cells (MNCs) may contribute to neurohumoral activation during disease states is unknown

5 contributes to exacerbated MNC activity and neurohumoral activation during disease states is unknown

6 We propose that neurohumoral activation early in the postinfarction peri

7 Neurohumoral activation follows a stepwise pattern, with

8 erapies that interrupt, or even reverse, the neurohumoral activation in heart failure hold the greate

9 s as an underlying mechanism contributing to neurohumoral activation in neurogenic hypertension.

10 eus of hypertensive rats that contributes to neurohumoral activation in this disease.

11 trophy induced by stresses such as aging and neurohumoral activation is an independent risk factor fo

12 However, the significance of this early neurohumoral activation is unclear.

13 Understanding this pattern of neurohumoral activation may aid in understanding the sig

14 el of reduced cardiac output that mimics the neurohumoral activation observed in congestive heart fai

15 lar Dysfunction (SOLVD) trial suggested that neurohumoral activation precedes the development of symp

16 The fundamental mechanisms underlying this neurohumoral activation remain unknown, however.

17 The hemodynamic abnormalities and neurohumoral activation that accompany congestive heart

18 ypothesize that biomarkers for inflammation, neurohumoral activation, and cardiac injury can predict

19 ncrease in serum biomarkers of inflammation, neurohumoral activation, and myocardial injury increased

20 Patients with the greatest amount of neurohumoral activation, as estimated by plasma norepine

21 t in atrial stretch, hemodynamic change, and neurohumoral activation, contributes partially to the at

22 ocardial energetic perturbations result from neurohumoral activation, increased adverse free fatty ac

23 triuretic peptide levels, renal dysfunction, neurohumoral activation, myocardial necrosis and fibrosi

24 pe I collagen levels, suggesting more severe neurohumoral activation, myocyte necrosis, and fibrosis.

25 CO3(-) secretion (DBS), a measure of mucosal neurohumoral activation.

26 such as insulin resistance, in part through neurohumoral activation.

27 ar hypertrophy but to possibly be related to neurohumoral activation.

28 urable effects on haemodynamic measurements, neurohumoral activity, and left-ventricular remodelling

29 We investigated the roles of 3 different neurohumoral agonists as possible i-NANC neurotransmitte

30 All 3 neurohumoral agonists produced relaxation (with no diffe

31 In HF, high Na(+) intake and neurohumoral alterations disrupt GAG structure, leading

32 H because of its known modulation of diverse neurohumoral and behavioral responses.

33 Its neurohumoral and hemodynamic profiles suggest possible a

34 We investigated the hemodynamic, neurohumoral, and myocardial blood flow responses to men

35 Although neurohumoral antagonism has successfully reduced heart f

36 mitigate aberrant metabolism include intense neurohumoral antagonism, limitation of diuretics, correc

37 Moreover, activation of the neurohumoral axis is unlikely to completely explain the

38 exposure as well as the consequence of this neurohumoral burst on cardiac stem cells (CSCs) are unkn

39 s associated with acute myocardial ischemia, neurohumoral changes, and genetic predisposition in the

40 ed experimental CHF based on hemodynamic and neurohumoral characteristics that closely mimic human di

41 ught of as a passive tissue that responds to neurohumoral control and inflammatory mediators.

42 these in the context of the ideas about the neurohumoral control of alimentary physiology that were

43 significant advances in our knowledge of the neurohumoral control of exocrine pancreatic secretion, e

44 ignaling may be important for development of neurohumoral control of intestinal motor reflexes.

45 In addition to new insights into the neurohumoral control of pancreatic secretion, these find

46 cle), and the relative absence of regulatory neurohumoral control of small vessel segments of the cir

47 s is their role in mechanical, chemical, and neurohumoral coupling processes that tune myofilament ac

48 ynaptic functions contributes to exacerbated neurohumoral drive in prevalent cardiovascular disorders

49 ta-PVN dendrites and ultimately leads to the neurohumoral dysfunction driving hypertension.

50 ect of hemodynamic stress or is secondary to neurohumoral effects in response to hemodynamic overload

51 a key (although presently undefined) role in neurohumoral excitation in humans with heart failure.

52 Neurohumoral excitation is organ specific, affecting the

53 Moreover, other stress-related neurohumoral factors appear to counter the repressive ef

54 When stimulated by a wide array of neurohumoral factors or when faced with an increase in v

55 During critical illness, neurohumoral factors, cytokines, endothelin, and atrial

56 e kinase strongly activated by integrins and neurohumoral factors.

57 of chronic oral ET-A receptor antagonism on neurohumoral function, renal hemodynamics, and sodium ex

58 These results, which demonstrate Ca(2+), neurohumoral, growth factor, cytokine, and developmental

59 to HF with reduced EF, large trials testing neurohumoral inhibition in HFpEF failed to reach a posit

60 ulation (EFS) in the presence and absence of neurohumoral inhibitors (tin protoporphyrin IX [SnPP IX]

61 In in vitro studies using neurohumoral inhibitors and tetrodotoxin and the use of

62 aemia reperfusion, myocardial infarction and neurohumoral injury, common causes of myocardial death a

63 eperfusion injury, myocardial infarction and neurohumoral injury, suggesting that pathological action

64 represents a neural substrate through which neurohumoral inputs are integrated within the forebrain

65 ddition to its modulation by reflex-mediated neurohumoral mechanisms, HR is also under the direct inf

66 sation in health and to explore the putative neurohumoral mechanisms.

67 le organ response in the absence of systemic neurohumoral mechanisms.

68 secretion are reviewed, with an emphasis on neurohumoral mechanisms.

69 ciated with alterations in potassium and the neurohumoral mediators of extrarenal potassium disposal

70 such altered membrane currents and a changed neurohumoral milieu creates a substrate that is highly s

71 2 diabetes mellitus alters the systemic and neurohumoral milieu, leading to changes in metabolism an

72 n contrast, CSCs were resistant to the acute neurohumoral overload.

73 ted to catecholamine stimulation to simulate neurohumoral overstimulation.

74 ents of Mozart's piano sonatas, we propose a neurohumoral pathway by which music might exert its seda

75 NaCl, regulate sympathetic drive and a novel neurohumoral pathway mediated by both brain and circulat

76 ither directly or through a leptin-regulated neurohumoral pathway.

77 d establish CaMKII as a nodal signal for the neurohumoral pathways associated with poor outcomes afte

78 iastolic function, deleterious activation of neurohumoral pathways, and high morbidity and mortality.

79 The cardiorenal and neurohumoral properties of mANP compared with ANP were a

80 To circumvent potential neurohumoral reflexes, cardiac efficiency was additional

81 review highlights recent discoveries in the neurohumoral regulation of pancreatic exocrine secretion

82 e in the generation of a systemic, polymodal neurohumoral response to a hyperosmotic challenge.

83 ation in plasma osmolality elicits a complex neurohumoral response, including an activation of the sy

84 imilar to its role in the counter-regulatory neurohumoral responses to glucoprivation.

85 udy examined the role of angiotensin II as a neurohumoral signal for the myogenic tone in the interna

86 The adult heart responds to excessive neurohumoral signaling and workload by a pathological gr

87 s in active and passive membrane properties, neurohumoral signaling, and genetic determinants that pr

88 growth in response to pressure overload and neurohumoral signaling, whereas mice lacking HDAC5, a cl

89 were subjected to ischemic injury or chronic neurohumoral stimulation and monitored for survival, car

90 f activation of ANP synthesis despite marked neurohumoral stimulation by the growth promoters ET and

91 ontribution of mechanical load compared with neurohumoral stimulation in vivo with specific focus on

92 this situation that have the least effect on neurohumoral stimulation of the pancreas.

93 2 abolishes the positive inotropic effect of neurohumoral stimulation with ET-1 and protects from its

94 Despite neurohumoral stimulation, LV mass index and myocyte diam

95 is in response to ischemic injury or chronic neurohumoral stimulation.

96 rption in isolated crypts that are devoid of neurohumoral stimulation.

97 rt processes plus fluid secretion induced by neurohumoral stimulation.

98 uring hemodynamic stress, catecholamines and neurohumoral stimuli may induce co-activation of G(q)-co

99 adult rat ventricular myocytes treated with neurohumoral stimuli such as angiotensin II (Ang II) and

100 e that in adult cardiomyocytes two important neurohumoral stimuli that induce hypertrophy, endothelin

101 hermore, HDAC phosphorylation in response to neurohumoral stimuli that induce hypertrophy, such as en

102 nse to increased ventricular wall tension or neurohumoral stimuli, the myocardium undergoes an adapti

103 ar energy status, is activated by stress and neurohumoral stimuli.

104 rophy is a common response to circulatory or neurohumoral stressors as a mechanism to augment contrac

105 with combined modulation of the ET and other neurohumoral systems in CHF are required.

106 econdary to vasodilatation and activation of neurohumoral systems.

107 econdary to vasodilatation and activation of neurohumoral systems.

108 econdary to vasodilatation and activation of neurohumoral systems.

109 proaches, such as antagonists to a number of neurohumoral targets (ie, endothelin [tezosentan], vasop

110 t to assess the primary preventive effect of neurohumoral therapy in high-risk diabetic patients sele

111 m (Na(+)) and fluid retention resulting from neurohumoral up-regulation.