Role of brain adrenoceptors in the corticortopin-releasing factor-induced central activation of sympatho-adrenomedullary outflow in rats

Yorimitsu, Mieko; Okada, Shoshiro; Yamaguchi, Naoko; Shimizu, Takahiro; Arai, Junichi; Yokotani, Kunihiko

doi:10.1016/j.lfs.2007.12.006

Cited by 7 publications

(5 citation statements)

References 52 publications

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“…Similar findings are presented in reports by Feldman and Weidenfeld, 36 Handley and Mithani, 37 Yorimitsu et al. 38 Jager et al. 39 stated that doxazosin had a negative effect on aldosterone secretion by adrenocortical cells porcine.…”

Section: Discussionsupporting

confidence: 85%

“…Shimizu 35 stated that agonists (NE and PE) of 36 Handley and Mithani, 37 Yorimitsu et al 38 Jager et al 39 stated that doxazosin had a negative effect on aldosterone secretion by adrenocortical cells porcine. Mulatero et al 40 found that an intravenous administration of doxazosin to patients with primary aldosteronism significantly lowered plasma aldosterone concentration.…”

Section: Discussionmentioning

confidence: 99%

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Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Kasacka

Piotrowska

Filipek

et al. 2015

Exp Biol Med (Maywood)

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Hypertension frequently results in severe complications in cardiovascular system and histopathological changes in the heart. To better understand the cellular processes and signaling pathways responsible for the proper functioning of the heart, we decided to check whether doxazosin affects the density of structures containing S100A6 and atrial natriuretic factor in the heart of spontaneously hypertensive rats. The aim of this study is to find differences in the density of the structures containing S100A6 and atrial natriuretic factor in the heart of spontaneously hypertensive rats treated with doxazosin compared to untreated animals. Fragments of heart were collected from five spontaneously hypertensive rats and five spontaneously hypertensive rats receiving doxazosin for six weeks (dose 0.1 mg per 1 kg of body weight). On the paraffin sections S100A6 and atrial natriuretic factor peptides were localized in the heart using immunohistochemistry. Positive immunohistochemical reaction for S100A6 was observed in atrial and ventricular cardiomyocytes and in the coronary vasculature. In the heart of hypertensive rats treated with doxazosin the S100A6 immunoreactivity was significantly lower compared to untreated animals. Immunodetection of atrial natriuretic factor in the heart of rats confirmed presence of peptide in atrial myocardium. Delicate atrial natriuretic factor-immunoreactivity was observed also in few ventricular cardiomyocytes. The atrial natriuretic factor-immunosignal was significantly weaker in hearts of hypertensive rats receiving doxazosin compared to spontaneously hypertensive rats untreated. Since we found that doxazosin reduces the levels of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats, it can be assumed that cardiovascular disorders that occur in hypertension may be associated with disturbances of cellular processes and signaling pathways.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Kasacka

Piotrowska

Filipek

et al. 2015

Exp Biol Med (Maywood)

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“…In addition the CRF signaling system also acts as a neurotransmitter/neuromodulator to coordinate the behavioral, immune, and visceral efferent limbs of the stress response 44,45,47-49. It does so via the activation of the locus coeruleus and its noradrenergic projections to the forebrain which contribute to arousal, alertness as well as the modulation of forebrain, hindbrain and spinal sites regulating the autonomic nervous system activity leading to the stimulation of the sympathetic nervous system and release of catecholamines,50-52 and sacral parasympathetic activity while decreasing vagal efferent output53-55 that influences immune and visceral function 56,57. In addition the brain CRF/CRF 1 signaling pathway is involved in stress-related induction of anxiety/depression44,45,58 and alterations of colonic motor and visceral pain while both central and peripheral CRF 2 receptor activation may exert a counteracting influence 59-63.…”

Section: Stress Pathways: Corticotropin Releasing Factor Signaling Asmentioning

confidence: 99%

Stress-Related Alterations of Visceral Sensation: Animal Models for Irritable Bowel Syndrome Study

Larauche¹,

Mulak²,

Taché³

2011

J Neurogastroenterol Motil

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Stressors of different psychological, physical or immune origin play a critical role in the pathophysiology of irritable bowel syndrome participating in symptoms onset, clinical presentation as well as treatment outcome. Experimental stress models applying a variety of acute and chronic exteroceptive or interoceptive stressors have been developed to target different periods throughout the lifespan of animals to assess the vulnerability, the trigger and perpetuating factors determining stress influence on visceral sensitivity and interactions within the brain-gut axis. Recent evidence points towards adequate construct and face validity of experimental models developed with respect to animals' age, sex, strain differences and specific methodological aspects such as non-invasive monitoring of visceromotor response to colorectal distension as being essential in successful identification and evaluation of novel therapeutic targets aimed at reducing stress-related alterations in visceral sensitivity. Underlying mechanisms of stress-induced modulation of visceral pain involve a combination of peripheral, spinal and supraspinal sensitization based on the nature of the stressors and dysregulation of descending pathways that modulate nociceptive transmission or stress-related analgesic response.

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“…Far beyond an exclusive neuroendocrine role, CRF, which is widely distributed outside of the hypothalamus (De Souza and Grigoriadis, 2002), also acts as a neurotransmitter/ neuromodulator to coordinate the behavioral, autonomic, immune, and visceral efferent limbs of the stress response (Bale and Vale, 2004; Caso et al, 2008; Friedman and Irwin, 1995; Taché et al, 2001). For instance brain CRF activates the sympathetic nervous system inducing the systemic release of catecholamines (adrenaline and noradrenaline) involved in the ”fight or flight” response (Tsatsanis et al, 2007; Usui et al, 2009; Yorimitsu et al, 2008). The locus coeruleus is also activated and its noradrenergic projections to the forebrain provide an additional source of noradrenaline which contributes to the arousal and alertness (Valentino et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Stress and visceral pain: From animal models to clinical therapies

Larauche

Mulak

Taché

2012

Experimental Neurology

181

207

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Epidemiological studies have implicated stress (psychosocial and physical) as a trigger of first onset or exacerbation of irritable bowel syndrome (IBS) symptoms of which visceral pain is an integrant landmark. A number of experimental acute or chronic exteroceptive or interoceptive stressors induce visceral hyperalgesia in rodents although recent evidence also points to stress-related visceral analgesia as established in the somatic pain field. Underlying mechanisms of stress-related visceral hypersensitivity may involve a combination of sensitization of primary afferents, central sensitization in response to input from the viscera and dysregulation of descending pathways that modulate spinal nociceptive transmission or analgesic response. Biochemical coding of stress involves the recruitment of corticotropin releasing factor (CRF) signaling pathways. Experimental studies established that activation of brain and peripheral CRF receptor subtype 1 plays a primary role in the development of stress-related delayed visceral hyperalgesia while subtype 2 activation induces analgesic response. In line with stress pathways playing a role in IBS, non-pharmacologic and pharmacologic treatment modalities aimed at reducing stress perception using a broad range of evidence-based mind-body interventions and centrally-targeted medications to reduce anxiety impact on brain patterns activated by visceral stimuli and dampen visceral pain.

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Role of brain adrenoceptors in the corticortopin-releasing factor-induced central activation of sympatho-adrenomedullary outflow in rats

Cited by 7 publications

References 52 publications

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Stress-Related Alterations of Visceral Sensation: Animal Models for Irritable Bowel Syndrome Study

Stress and visceral pain: From animal models to clinical therapies

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