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  1. AU="Ruginsk, Silvia G"
  2. AU="Aquilante, Francesco"
  3. AU="Dillon, Robert C"
  4. AU="Yuan Qu"
  5. AU="Dufour, A"
  6. AU="Hannus, Jill"
  7. AU="Rieber, Julia"
  8. AU="Gulmuradov, Tashpulat"
  9. AU="Romeu Fontanillas, Teresa"
  10. AU="Fleming, Renée"
  11. AU="Cao, Fang"
  12. AU="Sally J L Moore"
  13. AU="Moreno, Yolanda"
  14. AU="Vasiliy Ya. Kolyuchkin"

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  1. Artikel ; Online: Type 1 cannabinoid receptor modulates water deprivation-induced homeostatic responses.

    Ruginsk, Silvia G / Vechiato, Fernanda M V / Uchoa, Ernane T / Elias, Lucila L K / Antunes-Rodrigues, Jose

    American journal of physiology. Regulatory, integrative and comparative physiology

    2015  Band 309, Heft 11, Seite(n) R1358–68

    Abstract: The present study investigated the type 1 cannabinoid receptor (CB1R) as a potential candidate to mediate the homeostatic responses triggered by 24 h of water deprivation, which constitutes primarily a hydroelectrolytic challenge and also significantly ... ...

    Abstract The present study investigated the type 1 cannabinoid receptor (CB1R) as a potential candidate to mediate the homeostatic responses triggered by 24 h of water deprivation, which constitutes primarily a hydroelectrolytic challenge and also significantly impacts energy homeostasis. The present results demonstrated for the first time that CB1R mRNA expression is increased in the hypothalamus of water-deprived (WD) rats. Furthermore, the administration of ACEA, a CB1R selective agonist, potentiated WD-induced dipsogenic effect, whereas AM251, a CB1R antagonist, attenuated not only water but also salt intake in response to WD. In parallel with the modulation of thirst and salt appetite, we confirmed that CB1Rs are essential for the development of appropriated neuroendocrine responses. Although the administration of ACEA or AM251 did not produce any effects on WD-induced arginine vasopressin (AVP) secretion, oxytocin (OXT) plasma concentrations were significantly decreased in WD rats treated with ACEA. At the genomic level, ACEA significantly decreased AVP and OXT mRNA expression in the hypothalamus of WD rats, whereas AM251 potentiated both basal and WD-induced stimulatory effects on the transcription of AVP and OXT genes. In addition, we showed that water deprivation alone upregulated proopiomelanocortin, Agouti-related peptide, melanin-concentrating hormone, and orexin A mRNA levels in the hypothalamus, and that CB1Rs regulate main central peptidergic pathways controlling food intake, being that most of these effects were also significantly influenced by the hydration status. In conclusion, the present study demonstrated that CB1Rs participate in the homeostatic responses regulating fluid balance and energy homeostasis during water deprivation.
    Mesh-Begriff(e) Animals ; Appetite Regulation ; Arginine Vasopressin/genetics ; Arginine Vasopressin/metabolism ; Arterial Pressure ; Behavior, Animal ; Cannabinoid Receptor Agonists/pharmacology ; Cannabinoid Receptor Antagonists/pharmacology ; Energy Metabolism/drug effects ; Feeding Behavior ; Gene Expression Regulation ; Hypothalamus/drug effects ; Hypothalamus/metabolism ; Male ; Models, Animal ; Oxytocin/genetics ; Oxytocin/metabolism ; RNA, Messenger/metabolism ; Rats, Wistar ; Receptor, Cannabinoid, CB1/drug effects ; Receptor, Cannabinoid, CB1/genetics ; Receptor, Cannabinoid, CB1/metabolism ; Signal Transduction ; Sodium/blood ; Sodium Chloride, Dietary/administration & dosage ; Time Factors ; Transcription, Genetic ; Water Deprivation ; Water-Electrolyte Balance/drug effects
    Chemische Substanzen Cannabinoid Receptor Agonists ; Cannabinoid Receptor Antagonists ; Cnr1 protein, rat ; RNA, Messenger ; Receptor, Cannabinoid, CB1 ; Sodium Chloride, Dietary ; Arginine Vasopressin (113-79-1) ; Oxytocin (50-56-6) ; Sodium (9NEZ333N27)
    Sprache Englisch
    Erscheinungsdatum 2015-10-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00536.2014
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion.

    Ruginsk, Silvia G / Uchoa, Ernane T / Elias, Lucila Lk / Antunes-Rodrigues, Jose

    Clinical and experimental pharmacology & physiology

    2013  Band 40, Heft 10, Seite(n) 698–705

    Abstract: 1) The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1 R) antagonist (AM251) on the homeostatic ... ...

    Abstract (1) The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1 R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. (2) Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H-) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H-EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H-EVE group. (3) Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA-pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c-Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H-EVE. (4) The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1 R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic-pituitary-adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress-induced responses.
    Mesh-Begriff(e) Amidohydrolases/antagonists & inhibitors ; Animals ; Arachidonic Acids/administration & dosage ; Arachidonic Acids/pharmacology ; Benzamides/administration & dosage ; Benzamides/pharmacology ; Carbamates/administration & dosage ; Carbamates/pharmacology ; Endocannabinoids/administration & dosage ; Endocannabinoids/pharmacology ; Gene Expression Regulation/drug effects ; Infusions, Intraventricular ; Male ; Median Eminence/metabolism ; Neuroprotective Agents/administration & dosage ; Neuroprotective Agents/pharmacology ; Nitrates/metabolism ; Oxytocin/genetics ; Oxytocin/metabolism ; Piperidines/administration & dosage ; Piperidines/pharmacology ; Polyunsaturated Alkamides/administration & dosage ; Polyunsaturated Alkamides/pharmacology ; Pyrazoles/administration & dosage ; Pyrazoles/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats ; Rats, Wistar ; Receptor, Cannabinoid, CB1/antagonists & inhibitors ; Saline Solution, Hypertonic/adverse effects ; Vasopressins/genetics ; Vasopressins/metabolism
    Chemische Substanzen Arachidonic Acids ; Benzamides ; Carbamates ; Endocannabinoids ; Neuroprotective Agents ; Nitrates ; Piperidines ; Polyunsaturated Alkamides ; Pyrazoles ; RNA, Messenger ; Receptor, Cannabinoid, CB1 ; Saline Solution, Hypertonic ; cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester ; Vasopressins (11000-17-2) ; AM 251 (3I4FA44MAI) ; Oxytocin (50-56-6) ; Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-) ; anandamide (UR5G69TJKH)
    Sprache Englisch
    Erscheinungsdatum 2013-10
    Erscheinungsland Australia
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189277-0
    ISSN 1440-1681 ; 0305-1870 ; 0143-9294
    ISSN (online) 1440-1681
    ISSN 0305-1870 ; 0143-9294
    DOI 10.1111/1440-1681.12155
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Glial Cells Are Involved in ANG-II-Induced Vasopressin Release and Sodium Intake in Awake Rats.

    Flôr, Atalia F L / de Brito Alves, José L / França-Silva, Maria S / Balarini, Camille M / Elias, Lucila L K / Ruginsk, Silvia G / Antunes-Rodrigues, José / Braga, Valdir A / Cruz, Josiane C

    Frontiers in physiology

    2018  Band 9, Seite(n) 430

    Abstract: It is known that circulating angiotensin II (ANG-II) acts on the circumventricular organs (CVOs), which partially lack a normal blood-brain barrier, to stimulate pressor responses, vasopressin (AVP), and oxytocin (OT) secretion, as well as sodium and ... ...

    Abstract It is known that circulating angiotensin II (ANG-II) acts on the circumventricular organs (CVOs), which partially lack a normal blood-brain barrier, to stimulate pressor responses, vasopressin (AVP), and oxytocin (OT) secretion, as well as sodium and water intake. Although ANG-II type 1 receptors (AT1
    Sprache Englisch
    Erscheinungsdatum 2018-05-01
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2018.00430
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Increased exposure to sodium during pregnancy and lactation changes basal and induced behavioral and neuroendocrine responses in adult male offspring.

    Silva, Marcia S / Lúcio-Oliveira, Fabiana / Mecawi, Andre Souza / Almeida, Lucas F / Ruginsk, Silvia G / Greenwood, Michael P / Greenwood, Mingkwan / Vivas, Laura / Elias, Lucila L K / Murphy, David / Antunes-Rodrigues, José

    Physiological reports

    2017  Band 5, Heft 6

    Abstract: Excessive sodium ( ... ...

    Abstract Excessive sodium (Na
    Mesh-Begriff(e) Animals ; Behavior, Animal/drug effects ; Corticosterone/blood ; Drinking/drug effects ; Female ; Kidney/drug effects ; Kidney/metabolism ; Lactation/physiology ; Male ; Oxytocin/blood ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism ; Rats ; Rats, Wistar ; Sodium Chloride/pharmacology ; Urination/drug effects ; Urination/physiology ; Water Deprivation/physiology ; Water-Electrolyte Balance/drug effects
    Chemische Substanzen Sodium Chloride (451W47IQ8X) ; Oxytocin (50-56-6) ; Corticosterone (W980KJ009P)
    Sprache Englisch
    Erscheinungsdatum 2017-03-23
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.13210
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Chronic treatment with fluoxetine modulates vascular adrenergic responses by inhibition of pre- and post-synaptic mechanisms.

    Pereira, Camila A / Rodrigues, Fernanda L / Ruginsk, Silvia G / Zanotto, Camila Z / Rodrigues, José A / Duarte, Diego A / Costa-Neto, Claudio M / Resstel, Leonardo B / Carneiro, Fernando S / Tostes, Rita C

    European journal of pharmacology

    2017  Band 800, Seite(n) 70–80

    Abstract: Fluoxetine, a serotonin reuptake inhibitor (SSRI), has other effects in addition to blocking serotonin reuptake, including changes in the vasomotor tone. Whereas many studies focused on the acute effects of fluoxetine in the vasculature, its chronic ... ...

    Abstract Fluoxetine, a serotonin reuptake inhibitor (SSRI), has other effects in addition to blocking serotonin reuptake, including changes in the vasomotor tone. Whereas many studies focused on the acute effects of fluoxetine in the vasculature, its chronic effects are still limited. In the present study, we tested the hypothesis that chronic fluoxetine treatment modulates adrenergic vascular responses by interfering with post- and pre-synaptic mechanisms. Wistar rats were treated with vehicle (water) or chronic fluoxetine (10mg/kg/day) for 21 days. Blood pressure (BP) and heart rate were measured. Vascular reactivity was evaluated in perfused mesenteric arterial beds (MAB) and in mesenteric resistance arteries. Protein expression by western blot analysis or immunohistochemistry, β-arrestin recruitment by BRET and calcium influx by FLIPR assay. Fluoxetine treatment decreased phenylephrine (PE)-induced, but not electrical-field stimulation (EFS)-induced vasoconstriction. Fluoxetine-treated rats exhibited increased KCl-induced vasoconstriction, which was abolished by prazosin. Desipramine, an inhibitor of norepinephrine (NA) reuptake, increased EFS-induced vasoconstrictor response in vehicle-treated, but not in fluoxetine-treated rats. Chronic treatment did not alter vascular expression of α
    Mesh-Begriff(e) Animals ; Arterial Pressure/drug effects ; Calcium/metabolism ; Electric Stimulation ; Fluoxetine/pharmacology ; Heart Rate/drug effects ; Intracellular Space/drug effects ; Intracellular Space/metabolism ; Male ; Norepinephrine Plasma Membrane Transport Proteins/metabolism ; Potassium Chloride/pharmacology ; Rats ; Rats, Wistar ; Receptors, Adrenergic, alpha-1/metabolism ; Serotonin Uptake Inhibitors/pharmacology ; Signal Transduction/drug effects ; Sympathetic Nervous System/drug effects ; Sympathetic Nervous System/physiology ; Synapses/drug effects ; Time Factors ; Vasoconstriction/drug effects ; beta-Arrestins/metabolism
    Chemische Substanzen Norepinephrine Plasma Membrane Transport Proteins ; Receptors, Adrenergic, alpha-1 ; Serotonin Uptake Inhibitors ; beta-Arrestins ; Fluoxetine (01K63SUP8D) ; Potassium Chloride (660YQ98I10) ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2017-04-05
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2017.02.029
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Functional and structural changes in internal pudendal arteries underlie erectile dysfunction induced by androgen deprivation.

    Alves-Lopes, Rh Ure / Neves, Karla B / Silva, Marcondes Ab / Olivon, Vânia C / Ruginsk, Silvia G / Antunes-Rodrigues, José / Ramalho, Leandra Nz / Tostes, Rita C / Carneiro, Fernando Silva

    Asian journal of andrology

    2016  Band 19, Heft 5, Seite(n) 526–532

    Abstract: Androgen deficiency is strongly associated with erectile dysfunction (ED). Inadequate penile arterial blood flow is one of the major causes of ED. The blood flow to the corpus cavernosum is mainly derived from the internal pudendal arteries (IPAs); ... ...

    Abstract Androgen deficiency is strongly associated with erectile dysfunction (ED). Inadequate penile arterial blood flow is one of the major causes of ED. The blood flow to the corpus cavernosum is mainly derived from the internal pudendal arteries (IPAs); however, no study has evaluated the effects of androgen deprivation on IPA's function. We hypothesized that castration impairs IPAs reactivity and structure, contributing to ED. In our study, Wistar male rats, 8-week-old, were castrated and studied 30 days after orchiectomy. Functional and structural properties of rat IPAs were determined using wire and pressure myograph systems, respectively. Protein expression was determined by Western blot and immunohistochemistry. Plasma testosterone levels were determined using the IMMULITE 1000 Immunoassay System. Castrated rats exhibited impaired erectile function, represented by decreased intracavernosal pressure/mean arterial pressure ratio. IPAs from castrated rats exhibited decreased phenylephrine- and electrical field stimulation (EFS)-induced contraction and decreased acetylcholine- and EFS-induced vasodilatation. IPAs from castrated rats exhibited decreased internal diameter, external diameter, thickness of the arterial wall, and cross-sectional area. Castration decreased nNOS and α-actin expression and increased collagen expression, p38 (Thr180/Tyr182) phosphorylation, as well as caspase 3 cleavage. In conclusion, androgen deficiency is associated with impairment of IPA reactivity and structure and increased apoptosis signaling markers. Our findings suggest that androgen deficiency-induced vascular dysfunction is an event involving hypotrophic vascular remodeling of IPAs.
    Mesh-Begriff(e) Androgens/deficiency ; Animals ; Apoptosis Regulatory Proteins/metabolism ; Arterial Pressure ; Arteries/pathology ; Arteries/physiopathology ; Erectile Dysfunction/pathology ; Erectile Dysfunction/physiopathology ; Male ; Muscle Contraction/physiology ; Orchiectomy ; Penis/blood supply ; Penis/physiopathology ; Rats ; Rats, Wistar ; Testosterone/blood ; Vasodilation/drug effects
    Chemische Substanzen Androgens ; Apoptosis Regulatory Proteins ; Testosterone (3XMK78S47O)
    Sprache Englisch
    Erscheinungsdatum 2016-07-08
    Erscheinungsland China
    Dokumenttyp Journal Article
    ZDB-ID 2075824-8
    ISSN 1745-7262 ; 1008-682X
    ISSN (online) 1745-7262
    ISSN 1008-682X
    DOI 10.4103/1008-682X.173935
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Cardiovascular alterations at different stages of hypertension development during ethanol consumption: time-course of vascular and autonomic changes.

    Crestani, Carlos C / Lopes da Silva, Andréia / Scopinho, América A / Ruginsk, Silvia G / Uchoa, Ernane T / Correa, Fernando M A / Elias, Lucila L K / Antunes-Rodrigues, José / Resstel, Leonardo B M

    Toxicology and applied pharmacology

    2014  Band 280, Heft 2, Seite(n) 245–255

    Abstract: The aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of ... ...

    Abstract The aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their drinking water during four weeks. Ethanol effects were investigated at the end of each week. Mild hypertension was already observed at the first week of treatment, and a progressive blood pressure increase was observed along the evaluation period. Increased pressor response to phenylephrine was observed from first to fourth week. α1-Adrenoceptor protein in the mesenteric bed was enhanced at the first week, whereas β2-adrenoceptor protein in the aorta was reduced after the second week. In the third week, ethanol intake facilitated the depressor response to sodium nitroprusside, whereas in the fourth week it reduced nitrate content in aorta and increased it plasma. The bradycardic component of the baroreflex was impaired, whereas baroreflex tachycardia was enhanced at the third and fourth weeks. AT1A receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. Facilitated vascular responsiveness to nitric oxide seems to counteract ethanol-induced hypertension.
    Mesh-Begriff(e) Alcohol Drinking/adverse effects ; Alcohol Drinking/physiopathology ; Animals ; Baroreflex/drug effects ; Baroreflex/physiology ; Blood Pressure/drug effects ; Heart Rate/drug effects ; Hypertension/etiology ; Hypertension/physiopathology ; Male ; Natriuretic Peptide, C-Type/genetics ; Nitric Oxide/physiology ; Nitroprusside/pharmacology ; Phenylephrine/pharmacology ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1/genetics
    Chemische Substanzen Receptor, Angiotensin, Type 1 ; Natriuretic Peptide, C-Type (127869-51-6) ; Nitroprusside (169D1260KM) ; Phenylephrine (1WS297W6MV) ; Nitric Oxide (31C4KY9ESH)
    Sprache Englisch
    Erscheinungsdatum 2014-10-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2014.08.012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Time-course of neuroendocrine changes and its correlation with hypertension induced by ethanol consumption.

    Da Silva, Andreia Lopes / Ruginsk, Silvia G / Uchoa, Ernane Torres / Crestani, Carlos C / Scopinho, America A / Correa, Fernando Morgan A / De Martinis, Bruno Spinosa / Elias, Lucila Leico Kagohara / Resstel, Leonardo B / Antunes-Rodrigues, Jose

    Alcohol and alcoholism (Oxford, Oxfordshire)

    2013  Band 48, Heft 4, Seite(n) 495–504

    Abstract: Unlabelled: Ethanol (ETOH) consumption has been associated with endocrine and autonomic changes, including the development of hypertension. However, the sequence of pathophysiological events underlying the emergence of this effect is poorly understood.!# ...

    Abstract Unlabelled: Ethanol (ETOH) consumption has been associated with endocrine and autonomic changes, including the development of hypertension. However, the sequence of pathophysiological events underlying the emergence of this effect is poorly understood.
    Aims: This study aimed to establish a time-course correlation between neuroendocrine and cardiovascular changes contributing to the development of hypertension following ETOH consumption.
    Methods: Male adult Wistar rats were subjected to the intake of increasing ETOH concentrations in their drinking water (first week: 5%, second week: 10%, third and fourth weeks: 20% v/v).
    Results: ETOH consumption decreased plasma and urinary volumes, as well as body weight and fluid intake. Furthermore, plasma osmolality, plasma sodium and urinary osmolality were elevated in the ETOH-treated rats. ETOH intake also induced a progressive increase in the mean arterial pressure (MAP), without affecting heart rate. Initially, this increase in MAP was correlated with increased plasma concentrations of adrenaline and noradrenaline. After the second week of ETOH treatment, plasma catecholamines returned to basal levels, and incremental increases were observed in plasma concentrations of vasopressin (AVP) and angiotensin II (ANG II). Conversely, plasma oxytocin, atrial natriuretic peptide, prolactin and the hypothalamus-pituitary-adrenal axis components were not significantly altered by ETOH.
    Conclusions: Taken together, these results suggest that increased sympathetic activity may contribute to the early increase in MAP observed in ETOH-treated rats. However, the maintenance of this effect may be predominantly regulated by the long-term increase in the secretion of other circulating factors, such as AVP and ANG II, the secretion of both hormones being stimulated by the ETOH-induced dehydration.
    Mesh-Begriff(e) Alcohol Drinking/adverse effects ; Alcohol Drinking/metabolism ; Alcohol Drinking/physiopathology ; Angiotensin II/blood ; Animals ; Blood Pressure/drug effects ; Catecholamines/blood ; Heart Rate/drug effects ; Heart Rate/physiology ; Hypertension/blood ; Hypertension/chemically induced ; Hypertension/physiopathology ; Hypothalamo-Hypophyseal System/drug effects ; Male ; Pituitary-Adrenal System/drug effects ; Prolactin/blood ; Rats ; Vasopressins/blood
    Chemische Substanzen Catecholamines ; Vasopressins (11000-17-2) ; Angiotensin II (11128-99-7) ; Prolactin (9002-62-4)
    Sprache Englisch
    Erscheinungsdatum 2013-07
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604956-4
    ISSN 1464-3502 ; 0309-1635 ; 0735-0414
    ISSN (online) 1464-3502
    ISSN 0309-1635 ; 0735-0414
    DOI 10.1093/alcalc/agt040
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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