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Browsing by Author "Antunes-Rodrigues, José (7006219357)"

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    The effects of aging on biosynthetic processes in the rat hypothalamic osmoregulatory neuroendocrine system
    (2018)
    Greenwood, Michael P. (56346914300)
    ;
    Greenwood, Mingkwan (56081209100)
    ;
    Romanova, Elena V. (7103134553)
    ;
    Mecawi, Andre S. (19337525700)
    ;
    Paterson, Alex (57195424931)
    ;
    Sarenac, Olivera (23971098200)
    ;
    Japundžić-Žigon, Nina (6506302556)
    ;
    Antunes-Rodrigues, José (7006219357)
    ;
    Paton, Julian F.R. (55486090800)
    ;
    Sweedler, Jonathan V. (7102998068)
    ;
    Murphy, David (55479343600)
    Elderly people exhibit a diminished capacity to cope with osmotic challenges such as dehydration. We have undertaken a detailed molecular analysis of arginine vasopressin (AVP) biosynthetic processes in the supraoptic nucleus (SON) of the hypothalamus and secretory activity in the posterior pituitary of adult (3 months) and aged (18 months) rats, to provide a comprehensive analysis of age-associated changes to the AVP system. By matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis, we identified differences in pituitary peptides, including AVP, in adult and aged rats under both basal and dehydrated states. In the SON, increased Avp gene transcription, coincided with reduced Avp promoter methylation in aged rats. Based on transcriptome data, we have previously characterized a number of novel dehydration-induced regulatory factors involved in the response of the SON to osmotic cues. We found that some of these increase in expression with age, while dehydration-induced expression of these genes in the SON was attenuated in aged rats. In summary, we show that aging alters the rat AVP system at the genome, transcriptome, and peptidome levels. These alterations however did not affect circulating levels of AVP in basal or dehydrated states. © 2018 The Authors
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    Publication
    The effects of aging on biosynthetic processes in the rat hypothalamic osmoregulatory neuroendocrine system
    (2018)
    Greenwood, Michael P. (56346914300)
    ;
    Greenwood, Mingkwan (56081209100)
    ;
    Romanova, Elena V. (7103134553)
    ;
    Mecawi, Andre S. (19337525700)
    ;
    Paterson, Alex (57195424931)
    ;
    Sarenac, Olivera (23971098200)
    ;
    Japundžić-Žigon, Nina (6506302556)
    ;
    Antunes-Rodrigues, José (7006219357)
    ;
    Paton, Julian F.R. (55486090800)
    ;
    Sweedler, Jonathan V. (7102998068)
    ;
    Murphy, David (55479343600)
    Elderly people exhibit a diminished capacity to cope with osmotic challenges such as dehydration. We have undertaken a detailed molecular analysis of arginine vasopressin (AVP) biosynthetic processes in the supraoptic nucleus (SON) of the hypothalamus and secretory activity in the posterior pituitary of adult (3 months) and aged (18 months) rats, to provide a comprehensive analysis of age-associated changes to the AVP system. By matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis, we identified differences in pituitary peptides, including AVP, in adult and aged rats under both basal and dehydrated states. In the SON, increased Avp gene transcription, coincided with reduced Avp promoter methylation in aged rats. Based on transcriptome data, we have previously characterized a number of novel dehydration-induced regulatory factors involved in the response of the SON to osmotic cues. We found that some of these increase in expression with age, while dehydration-induced expression of these genes in the SON was attenuated in aged rats. In summary, we show that aging alters the rat AVP system at the genome, transcriptome, and peptidome levels. These alterations however did not affect circulating levels of AVP in basal or dehydrated states. © 2018 The Authors
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    Publication
    Vasopressin and v1br gene expression is increased in the hypothalamic pvn of borderline hypertensive rats
    (2020)
    Savić, Bojana (57216800047)
    ;
    Martin, Andrew (56393484400)
    ;
    Mecawi, Andre Souza (19337525700)
    ;
    Bukumirić, Zoran (36600111200)
    ;
    Antunes-Rodrigues, José (7006219357)
    ;
    Murphy, David (55479343600)
    ;
    Šarenac, Olivera (23971098200)
    ;
    Japundžić–Žigon, Nina (57216800734)
    Vasopressin (VP) is a neurohypophyseal peptide best known for its role in maintaining osmotic and cardiovascular homeostasis. The main sources of VP are the supraoptic and paraventricular (PVN) nuclei of the hypothalamus, which coexpress the vasopressin V1a and V1b receptors (V1aR and V1bR). Here, we investigated the level of expression of VP and VP receptors in the PVN of borderline hypertensive rats (BHRs), a key integrative nucleus for neuroendocrine cardiovascular control. Experiments were performed in male BHRs and Wistar rats (WRs) equipped with a radiotelemetry device for continuous hemodynamic recording under baseline conditions and after saline load without or with stress. Autonomic control of the circulation was evaluated by spectral analysis of blood pressure (BP) and heart rate (HR) variability and baroreceptor reflex sensitivity (BRS) using the sequence method. Plasma VP was determined by radioimmunoassay, and VP, V1aR, and V1bR gene expression was determined by RT-qPCR. Under baseline conditions, BHRs had higher BP, lower HR, and stronger BRS than WRs. BP and HR variability was unchanged. In the PVN, overexpression of the VP and V1bR genes was found, and plasma VP was increased. Saline load downregulated V1bR mRNA expression without affecting VP mRNA expression or plasma VP and BP. Adding stress increased BP, HR, and low-frequency sympathetic spectral markers and decreased plasma VP without altering the level of expression of VP and VP receptors in the PVN. It follows that overexpression of VP and V1bR in the PVN is a characteristic trait of BHRs and that sympathetic hyperactivity underlies stress-induced hypertension. © 2020, The Japanese Society of Hypertension.
  • Loading...
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    Publication
    Vasopressin and v1br gene expression is increased in the hypothalamic pvn of borderline hypertensive rats
    (2020)
    Savić, Bojana (57216800047)
    ;
    Martin, Andrew (56393484400)
    ;
    Mecawi, Andre Souza (19337525700)
    ;
    Bukumirić, Zoran (36600111200)
    ;
    Antunes-Rodrigues, José (7006219357)
    ;
    Murphy, David (55479343600)
    ;
    Šarenac, Olivera (23971098200)
    ;
    Japundžić–Žigon, Nina (57216800734)
    Vasopressin (VP) is a neurohypophyseal peptide best known for its role in maintaining osmotic and cardiovascular homeostasis. The main sources of VP are the supraoptic and paraventricular (PVN) nuclei of the hypothalamus, which coexpress the vasopressin V1a and V1b receptors (V1aR and V1bR). Here, we investigated the level of expression of VP and VP receptors in the PVN of borderline hypertensive rats (BHRs), a key integrative nucleus for neuroendocrine cardiovascular control. Experiments were performed in male BHRs and Wistar rats (WRs) equipped with a radiotelemetry device for continuous hemodynamic recording under baseline conditions and after saline load without or with stress. Autonomic control of the circulation was evaluated by spectral analysis of blood pressure (BP) and heart rate (HR) variability and baroreceptor reflex sensitivity (BRS) using the sequence method. Plasma VP was determined by radioimmunoassay, and VP, V1aR, and V1bR gene expression was determined by RT-qPCR. Under baseline conditions, BHRs had higher BP, lower HR, and stronger BRS than WRs. BP and HR variability was unchanged. In the PVN, overexpression of the VP and V1bR genes was found, and plasma VP was increased. Saline load downregulated V1bR mRNA expression without affecting VP mRNA expression or plasma VP and BP. Adding stress increased BP, HR, and low-frequency sympathetic spectral markers and decreased plasma VP without altering the level of expression of VP and VP receptors in the PVN. It follows that overexpression of VP and V1bR in the PVN is a characteristic trait of BHRs and that sympathetic hyperactivity underlies stress-induced hypertension. © 2020, The Japanese Society of Hypertension.

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