Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen

Campos, Luciana Aparecida; Iliescu, Radu; Fontes, Marco Antônio Peliky; Schlegel, Wolfgang-Peter; Bäder, Michael; Baltatu, Ovidiu Constantin

doi:10.1152/ajpheart.01145.2005

Cited by 8 publications

(10 citation statements)

References 42 publications

(41 reference statements)

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“…Ang II signaling in the brain modulates reflex control of heart rate and sympathetic outflow (Dampney et al, 2007; Carlson and Wyss, 2008). Studies from our group provide evidence that a permanent inhibition of brain RAS may cause a decreased basal sympathetic outflow, as it has been observed in TGR(ASrAOGEN) rats (Campos et al, 2006a; Parrish et al, 2008). Power spectral analysis of heart rate and blood pressure indicates an altered autonomic nervous system activity with a dominance of vagal tone over sympathetic tone and exaggerated spontaneous baroreflex sensitivity (Baltatu et al, 2001).…”

supporting

confidence: 62%

“…Power spectral analysis of heart rate and blood pressure indicates an altered autonomic nervous system activity with a dominance of vagal tone over sympathetic tone and exaggerated spontaneous baroreflex sensitivity (Baltatu et al, 2001). As a consequence to a diminished basal activity of sympathetic nervous system, the hearts of TGR(ASrAOGEN) exhibit an increased sensitivity to β-receptor agonists (Campos et al, 2006a; Parrish et al, 2008). …”

mentioning

confidence: 99%

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Brain Renin–Angiotensin System in Hypertension, Cardiac Hypertrophy, and Heart Failure

Campos¹,

Bäder²,

Baltatu³

2012

Front. Physio.

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Brain renin–angiotensin system (RAS) is significantly involved in the roles of the endocrine RAS in cardiovascular regulation. Our studies indicate that the brain RAS participates in the development of cardiac hypertrophy and fibrosis through sympathetic activation. Inhibition of sympathetic hyperactivity after myocardial infarction through suppression of the brain RAS appears beneficial. Furthermore, the brain RAS modulates the cardiovascular and fluid–electrolyte homeostasis not only by interacting with the autonomic nervous system but also by modulating hypothalamic–pituitary axis and vasopressin release. The brain RAS is also involved in the modulation of circadian rhythms of arterial pressure, contributing to non-dipping hypertension. We conclude that the brain RAS in pathophysiological states interacts synergistically with the chronically overactive RAS through a positive biofeedback in order to maintain a state of alert in diseased conditions, such as cardiac hypertrophy and failure. Therefore, targeting brain RAS with drugs such as renin or angiotensin converting enzyme inhibitors or receptor blockers having increased brain penetrability could be of advantage.

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confidence: 62%

mentioning

confidence: 99%

Brain Renin–Angiotensin System in Hypertension, Cardiac Hypertrophy, and Heart Failure

Campos¹,

Bäder²,

Baltatu³

2012

Front. Physio.

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“…The chronic stimulation of the -AR by the administration of isoproterenol 15 induces the increase of cardiac mass, cardiomyocytes, myocardial fibrosis and progressive dysfunction, which culminates in heart failure. Acutely, the activation of 1 -AR increases the contractility mediated by the Gq protein activation.…”

Section: Pressure And/or Volume Overloadmentioning

confidence: 99%

Fatores e mecanismos envolvidos na hipertrofia ventricular esquerda e o papel anti-hipertrófico do óxido nítrico

Garcia¹,

Incerpi²

2008

Arq. Bras. Cardiol.

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SummaryThe left ventricular hypertrophy (LVH) occurs in response to the hemodynamic overload in some physiological and pathological conditions. However, it has not been completely elucidated whether the primary stimulation for the hypertrophy is the mechanical stretching of the heart, neurohumoral factors, or even the interaction of both. These factors are translated inside the cell as biochemical alterations that lead to the activation of second (cytosolic) and third (nuclear) messengers that will act in the cell nucleus, regulating transcription, and will finally determine the genic expression that induces LVH. The LVH is characterized by structural alterations due to the increase in the cardiomyocyte dimensions, the proliferation of the interstitial connective tissue and the rarefaction of the coronary microcirculation. Recently, nitric oxide (• NO) has appeared as an important regulator of cardiac remodeling, specifically recognized as an anti-hypertrophic mediator. Some studies have demonstrated the cellular targets, the anti-hypertrophic signaling pathways and the functional role of• NO. Thus, the LVH seems to develop as a result of the loss of the balance between the pro and the antihypertrophic signaling pathways. This new knowledge about the pro and anti-hypertrophic signaling pathways will allow the development of new strategies in the treatment of pathological LVH.

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“…The baroreflex sensitivity (BRS) is a measure of baroreflex function and is defined as alterations in beat-to-beat interval (milliseconds) per unit change in blood pressure (mm Hg). BRS is influenced by various neuroendocrine systems, including central renin angiotensin system (Campos et al, 2004, 2006a) and melatonin (Campos et al, 2013b). Interplay between these systems might be responsible for the circadian alterations in cardiovascular function (Baltatu et al, 2002; Campos et al, 2006b, 2013a).…”

Section: Introductionmentioning

confidence: 99%

Mathematical biomarkers for the autonomic regulation of cardiovascular system

Campos¹,

Pereira²,

Muralikrishna³

et al. 2013

Front. Physiol.

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Heart rate and blood pressure are the most important vital signs in diagnosing disease. Both heart rate and blood pressure are characterized by a high degree of short term variability from moment to moment, medium term over the normal day and night as well as in the very long term over months to years. The study of new mathematical algorithms to evaluate the variability of these cardiovascular parameters has a high potential in the development of new methods for early detection of cardiovascular disease, to establish differential diagnosis with possible therapeutic consequences. The autonomic nervous system is a major player in the general adaptive reaction to stress and disease. The quantitative prediction of the autonomic interactions in multiple control loops pathways of cardiovascular system is directly applicable to clinical situations. Exploration of new multimodal analytical techniques for the variability of cardiovascular system may detect new approaches for deterministic parameter identification. A multimodal analysis of cardiovascular signals can be studied by evaluating their amplitudes, phases, time domain patterns, and sensitivity to imposed stimuli, i.e., drugs blocking the autonomic system. The causal effects, gains, and dynamic relationships may be studied through dynamical fuzzy logic models, such as the discrete-time model and discrete-event model. We expect an increase in accuracy of modeling and a better estimation of the heart rate and blood pressure time series, which could be of benefit for intelligent patient monitoring. We foresee that identifying quantitative mathematical biomarkers for autonomic nervous system will allow individual therapy adjustments to aim at the most favorable sympathetic-parasympathetic balance.

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Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen

Cited by 8 publications

References 42 publications

Brain Renin–Angiotensin System in Hypertension, Cardiac Hypertrophy, and Heart Failure

Brain Renin–Angiotensin System in Hypertension, Cardiac Hypertrophy, and Heart Failure

Fatores e mecanismos envolvidos na hipertrofia ventricular esquerda e o papel anti-hipertrófico do óxido nítrico

Mathematical biomarkers for the autonomic regulation of cardiovascular system

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