LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 21

Search options

  1. Article ; Online: Stimulation of aldosterone synthesis by angiotensin II in the brain: support for positive feedback in hypertension?

    Scheuer, Deborah A

    Hypertension (Dallas, Tex. : 1979)

    2013  Volume 62, Issue 3, Page(s) 459–460

    MeSH term(s) Aldosterone/metabolism ; Animals ; Brain/metabolism ; Corticosterone/metabolism ; Hypertension/metabolism ; Male
    Chemical Substances Aldosterone (4964P6T9RB) ; Corticosterone (W980KJ009P)
    Language English
    Publishing date 2013-07-15
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.113.01649
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Adrenal corticosteroid effects in the central nervous system on long-term control of blood pressure.

    Scheuer, Deborah A

    Experimental physiology

    2010  Volume 95, Issue 1, Page(s) 10–12

    MeSH term(s) Adrenal Cortex Hormones/physiology ; Adrenal Glands/physiology ; Animals ; Blood Pressure/physiology ; Central Nervous System/physiology ; Congresses as Topic ; Humans ; Time Factors
    Chemical Substances Adrenal Cortex Hormones
    Language English
    Publishing date 2010-01-10
    Publishing country England
    Document type Comment ; Introductory Journal Article
    ZDB-ID 1016295-1
    ISSN 1469-445X ; 0958-0670
    ISSN (online) 1469-445X
    ISSN 0958-0670
    DOI 10.1113/expphysiol.2008.045484
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Pathways to hypertension.

    Scheuer, Deborah A

    The Journal of physiology

    2008  Volume 586, Issue 21, Page(s) 5033

    MeSH term(s) Humans ; Hypertension/etiology ; Hypertension/metabolism ; Hypothalamus/physiology ; Osmolar Concentration ; Paraventricular Hypothalamic Nucleus/physiology ; Proto-Oncogene Proteins c-fos ; Sympathetic Nervous System/physiology
    Chemical Substances Proto-Oncogene Proteins c-fos
    Language English
    Publishing date 2008-11-01
    Publishing country England
    Document type Comment ; Journal Article
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/jphysiol.2008.163014
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Regulation of the stress response in rats by central actions of glucocorticoids.

    Scheuer, Deborah A

    Experimental physiology

    2009  Volume 95, Issue 1, Page(s) 26–31

    Abstract: Chronic stress causes elevations in glucocorticoid secretion and also increases the incidence of hypertension and other manifestations of cardiovascular disease. The extent to which the elevated glucocorticoids mediate the stress-associated increase in ... ...

    Abstract Chronic stress causes elevations in glucocorticoid secretion and also increases the incidence of hypertension and other manifestations of cardiovascular disease. The extent to which the elevated glucocorticoids mediate the stress-associated increase in cardiovascular disease risk is unknown. Chronically elevated glucocorticoids can cause hypertension by acting in the periphery, but their effects within the brain on blood pressure regulation remain largely unexplored. We developed a method to produce selective chronic increases in the endogenous glucocorticoid corticosterone or the glucocorticoid receptor antagonist mifepristone within the hindbrain region, which includes a key cardiovascular regulatory area, the nucleus of the solitary tract (NTS). Experiments were performed in male Sprague-Dawley, Wistar-Kyoto (WKY) and borderline hypertensive rats (BHR). The results indicate that elevated exogenous corticosterone can act within the hindbrain to enhance the arterial pressure response to novel restraint stress and to reduce the gain and increase the mid-point of the arterial baroreflex. Basal levels of endogenous corticosterone have no effect on the arterial pressure response to stress in normotensive rats but enhance this response in BHR. Chronic stress-induced increases in baseline corticosterone enhance the arterial pressure response to stress in BHR but attenuate the adaptation of the response in WKY rats. Furthermore, an elevated corticosterone concentration within the hindbrain is necessary but not sufficient to cause glucocorticoid-induced hypertension. The effects of corticosterone within the hindbrain on blood pressure regulation are mediated in part by the glucocortiocid receptor, but are also likely to involve mineralocorticoid receptor-mediated effects and NTS catecholaminergic neurons. These data support the hypothesis that elevated glucocorticoids acting within the brain probably contribute to the adverse effects of stress on cardiovascular health in susceptible people.
    MeSH term(s) Animals ; Blood Pressure/physiology ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Glucocorticoids/metabolism ; Glucocorticoids/physiology ; Humans ; Rats ; Receptors, Glucocorticoid/physiology ; Rhombencephalon/metabolism ; Stress, Physiological/physiology
    Chemical Substances Glucocorticoids ; Receptors, Glucocorticoid
    Language English
    Publishing date 2009-09-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1016295-1
    ISSN 1469-445X ; 0958-0670
    ISSN (online) 1469-445X
    ISSN 0958-0670
    DOI 10.1113/expphysiol.2008.045971
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: Stress-induced corticosterone secretion covaries with working memory in aging.

    McQuail, Joseph A / Krause, Eric G / Setlow, Barry / Scheuer, Deborah A / Bizon, Jennifer L

    Neurobiology of aging

    2018  Volume 71, Page(s) 156–160

    Abstract: A substantial literature details the relationship between age-related changes to the hypothalamic-pituitary-adrenal axis and deterioration of mnemonic functions that depend on the hippocampus. The relationship between adrenocortical status and other ... ...

    Abstract A substantial literature details the relationship between age-related changes to the hypothalamic-pituitary-adrenal axis and deterioration of mnemonic functions that depend on the hippocampus. The relationship between adrenocortical status and other forms of memory that depend on the prefrontal cortex is less well understood in the context of advanced age. Here, we characterized performance of young adult and aged F344 rats on a prefrontal cortex-dependent working memory task and subsequently measured corticosterone (CORT) levels over the diurnal cycle and during exposure to an acute stressor. Our analyses revealed that aged rats with better working memory mounted a greater CORT response during acute stress exposure than either young adults or age-matched rats with impaired working memory. We also observed that age-related elevation of basal CORT levels is not associated with working memory performance. Jointly, these data reveal that the hypothalamic-pituitary-adrenal axis-mediated response to acute stress is positively associated with working memory in aging.
    MeSH term(s) Aging ; Animals ; Choice Behavior ; Corticosterone/blood ; Hypothalamo-Hypophyseal System/metabolism ; Male ; Memory, Short-Term/physiology ; Pituitary-Adrenal System/metabolism ; Prefrontal Cortex/physiology ; Rats, Inbred F344 ; Restraint, Physical ; Stress, Psychological/blood ; Stress, Psychological/psychology
    Chemical Substances Corticosterone (W980KJ009P)
    Language English
    Publishing date 2018-07-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604505-4
    ISSN 1558-1497 ; 0197-4580
    ISSN (online) 1558-1497
    ISSN 0197-4580
    DOI 10.1016/j.neurobiolaging.2018.07.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: Brain-derived neurotrophic factor modulates angiotensin signaling in the hypothalamus to increase blood pressure in rats.

    Erdos, Benedek / Backes, Iara / McCowan, Michael L / Hayward, Linda F / Scheuer, Deborah A

    American journal of physiology. Heart and circulatory physiology

    2015  Volume 308, Issue 6, Page(s) H612–22

    Abstract: Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) in response to hypertensive stimuli including stress and hyperosmolarity. However, it is unclear whether BDNF in the PVN contributes to ...

    Abstract Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) in response to hypertensive stimuli including stress and hyperosmolarity. However, it is unclear whether BDNF in the PVN contributes to increases in blood pressure (BP). We tested the hypothesis that increased BDNF levels within the PVN would elevate baseline BP and heart rate (HR) and cardiovascular stress responses by altering central angiotensin signaling. BP was recorded using radiotelemetry in male Sprague-Dawley rats after bilateral PVN injections of adeno-associated viral vectors expressing green fluorescent protein (GFP) or myc epitope-tagged BDNF fusion protein. Cardiovascular responses to acute stress were evaluated 3 to 4 wk after injections. Additional GFP and BDNF-treated animals were equipped with osmotic pumps for intracerebroventricular infusion of saline or the angiotensin type-1 receptor (AT1R) inhibitor losartan (15 μg·0.5 μl(-1)·h(-1)). BDNF treatment significantly increased baseline BP (121 ± 3 mmHg vs. 99 ± 2 mmHg in GFP), HR (394 ± 9 beats/min vs. 314 ± 4 beats/min in GFP), and sympathetic tone indicated by HR- and BP-variability analysis and adrenomedullary tyrosine hydroxylase protein expression. In contrast, body weight and BP elevations to acute stressors decreased. BDNF upregulated AT1R mRNA by ∼80% and downregulated Mas receptor mRNA by ∼50% in the PVN, and losartan infusion partially inhibited weight loss and increases in BP and HR in BDNF-treated animals without any effect in GFP rats. Our results demonstrate that BDNF overexpression in the PVN results in sympathoexcitation, BP and HR elevations, and weight loss that are mediated, at least in part, by modulating angiotensin signaling in the PVN.
    MeSH term(s) Adrenal Medulla/metabolism ; Angiotensin II Type 1 Receptor Blockers/administration & dosage ; Angiotensins/metabolism ; Animals ; Blood Pressure/drug effects ; Body Weight ; Brain-Derived Neurotrophic Factor/biosynthesis ; Brain-Derived Neurotrophic Factor/genetics ; Cardiovascular System/innervation ; Dependovirus/genetics ; Gene Transfer Techniques ; Genetic Vectors ; Heart Rate ; Hypertension/genetics ; Hypertension/metabolism ; Hypertension/physiopathology ; Infusions, Intraventricular ; Male ; Paraventricular Hypothalamic Nucleus/drug effects ; Paraventricular Hypothalamic Nucleus/metabolism ; Proto-Oncogene Proteins/metabolism ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1/drug effects ; Receptor, Angiotensin, Type 1/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Renin-Angiotensin System/drug effects ; Signal Transduction/drug effects ; Stress, Psychological/metabolism ; Stress, Psychological/physiopathology ; Sympathetic Nervous System/drug effects ; Sympathetic Nervous System/metabolism ; Sympathetic Nervous System/physiopathology ; Time Factors ; Tyrosine 3-Monooxygenase/metabolism ; Up-Regulation
    Chemical Substances Angiotensin II Type 1 Receptor Blockers ; Angiotensins ; Brain-Derived Neurotrophic Factor ; Proto-Oncogene Proteins ; Receptor, Angiotensin, Type 1 ; Receptors, G-Protein-Coupled ; proto-oncogene proteins c-mas-1 ; Tyrosine 3-Monooxygenase (EC 1.14.16.2)
    Language English
    Publishing date 2015-01-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00776.2014
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats.

    Daubert, Daisy L / McCowan, Michael / Erdos, Benedek / Scheuer, Deborah A

    The Journal of physiology

    2012  Volume 590, Issue 19, Page(s) 4881–4895

    Abstract: Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS ... ...

    Abstract Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS catecholaminergic neurons attenuate psychological stress-induced increases in blood pressure and promote neuroendocrine activation in response to psychological stress.Anti-dopamine-β-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into the NTS to lesion catecholaminergic neurons in male Sprague-Dawley rats, and 17 days later the rats were subjected to 60 min of restraint stress for five consecutive days. DSAP treatment significantly enhanced the integrated increase in mean arterial pressure during restraint on the first (800 ± 128 and 1115 ± 116 mmHg (min) for saline- and DSAP-treated rats) and fifth days (655 ± 116 and 1035 ± 113 mmHg (min) for saline- and DSAP-treated rats; P<0.01 for overall effect of DSAP treatment) of restraint. In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in DSAP-treated compared with saline-treated rats (25.9 ± 7 compared with 46.8 ± 7 μg dl(-1) for DSAP- and saline-treated rats; P <0.05). DSAP treatment also significantly reduced baseline plasma adrenaline concentration (403 ± 69 compared with 73 ± 29 pg ml(-1) for saline- and DSAP-treated rats), but did not alter the magnitude of the adrenaline response to restraint. The data suggest that NTS catecholaminergic neurons normally inhibit the arterial pressure response, but help maintain the corticosterone response to restraint stress.
    MeSH term(s) Animals ; Antibodies/chemistry ; Antibodies/pharmacology ; Blood Pressure/physiology ; Corticosterone/blood ; Dopamine beta-Hydroxylase/physiology ; Epinephrine/blood ; Heart Rate/physiology ; Male ; Neurons/physiology ; Norepinephrine/physiology ; Rats ; Rats, Sprague-Dawley ; Restraint, Physical ; Ribosome Inactivating Proteins, Type 1/chemistry ; Ribosome Inactivating Proteins, Type 1/pharmacology ; Saporins ; Solitary Nucleus/physiopathology ; Stress, Psychological/physiopathology
    Chemical Substances Antibodies ; Ribosome Inactivating Proteins, Type 1 ; Dopamine beta-Hydroxylase (EC 1.14.17.1) ; Saporins (EC 3.2.2.22) ; Corticosterone (W980KJ009P) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
    Language English
    Publishing date 2012-07-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/jphysiol.2012.232314
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate.

    Bechtold, Andrea G / Scheuer, Deborah A

    American journal of physiology. Regulatory, integrative and comparative physiology

    2005  Volume 290, Issue 4, Page(s) R1003–11

    Abstract: Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, ... ...

    Abstract Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, we tested the hypothesis that prolonged activation of DHB Cort receptors increases the midpoint and reduces the gain of arterial baroreflex control of heart rate in conscious rats. Small (3-4 mg) pellets of Cort (DHB Cort) or Silastic (DHB Sham) were placed on the surface of the DHB, or Cort was administered systemically by placing a Cort pellet on the surface of the dura (Dura Cort). Baroreflex control of heart rate was determined in conscious male Sprague Dawley rats on each of 4 days after initiation of treatment. Plots of arterial pressure vs. heart rate were analyzed using a four-parameter logistic function. After 3 days of treatment, the arterial pressure midpoint for baroreflex control of heart rate was increased in DHB Cort rats (123 +/- 2 mmHg) relative to both DHB Sham (108 +/- 3 mmHg) and Dura Cort rats (109 +/- 2 mmHg, P < 0.05). On day 4, baseline arterial pressure was greater in DHB Cort (112 +/- 2 mmHg) compared with DHB Sham (105 +/- 2 mmHg) and Dura Cort animals (106 +/- 2 mmHg, P < 0.05), and the arterial pressure midpoint was significantly greater than mean arterial pressure in the DHB Cort group only. Also on day 4, maximum baroreflex gain was reduced in DHB Cort (2.72 +/- 0.12 beats x min(-1) x mmHg(-1)) relative to DHB Sham and Dura Cort rats (3.51 +/- 0.28 and 3.37 +/- 0.27 beats x min(-1) x mmHg(-1), P < 0.05). We conclude that Cort acts in the DHB to increase the midpoint and reduce the gain of the heart rate baroreflex function.
    MeSH term(s) Animals ; Arteries/physiology ; Baroreflex/drug effects ; Baroreflex/physiology ; Carrier Proteins/pharmacology ; Catheters, Indwelling ; Consciousness ; Dimethylpolysiloxanes/pharmacology ; Glucocorticoids/pharmacology ; Heart Rate/drug effects ; Male ; Neuropeptides/pharmacology ; Pressoreceptors/metabolism ; Rats ; Rats, Sprague-Dawley ; Rhombencephalon/physiology ; Silicones/pharmacology
    Chemical Substances CORT protein, human ; Carrier Proteins ; Dimethylpolysiloxanes ; Glucocorticoids ; Neuropeptides ; Silicones ; baysilon (63148-62-9)
    Language English
    Publishing date 2005-11-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00345.2005
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: Elevated corticosterone in the dorsal hindbrain increases plasma norepinephrine and neuropeptide Y, and recruits a vasopressin response to stress.

    Daubert, Daisy L / Looney, Benjamin M / Clifton, Rebekah R / Cho, Jake N / Scheuer, Deborah A

    American journal of physiology. Regulatory, integrative and comparative physiology

    2014  Volume 307, Issue 2, Page(s) R212–24

    Abstract: Repeated stress and chronically elevated glucocorticoids cause exaggerated cardiovascular responses to novel stress, elevations in baseline blood pressure, and increased risk for cardiovascular disease. We hypothesized that elevated corticosterone (Cort) ...

    Abstract Repeated stress and chronically elevated glucocorticoids cause exaggerated cardiovascular responses to novel stress, elevations in baseline blood pressure, and increased risk for cardiovascular disease. We hypothesized that elevated corticosterone (Cort) within the dorsal hindbrain (DHB) would: 1) enhance arterial pressure and neuroendocrine responses to novel and repeated restraint stress, 2) increase c-Fos expression in regions of the brain involved in sympathetic stimulation during stress, and 3) recruit a vasopressin-mediated blood pressure response to acute stress. Small pellets made of 10% Cort were implanted on the surface of the DHB in male Sprague-Dawley rats. Blood pressure was measured by radiotelemetry. Cort concentration was increased in the DHB in Cort-treated compared with Sham-treated rats (60 ± 15 vs. 14 ± 2 ng Cort/g of tissue, P < 0.05). DHB Cort significantly increased the integrated arterial pressure response to 60 min of restraint stress on days 6, 13, and 14 following pellet implantation (e.g., 731 ± 170 vs. 1,204 ± 68 mmHg/60 min in Sham- vs. Cort-treated rats, day 6, P < 0.05). Cort also increased baseline blood pressure by day 15 (99 ± 2 vs. 108 ± 3 mmHg for Sham- vs. Cort-treated rats, P < 0.05) and elevated baseline plasma norepinephrine and neuropeptide Y concentrations. Cort significantly enhanced stress-induced c-Fos expression in vasopressin-expressing neurons in the paraventricular nucleus of the hypothalamus, and blockade of peripheral vasopressin V1 receptors attenuated the effect of DHB Cort to enhance the blood pressure response to restraint. These data indicate that glucocorticoids act within the DHB to produce some of the adverse cardiovascular consequences of chronic stress, in part, by a peripheral vasopressin-dependent mechanism.
    MeSH term(s) Animals ; Blood Pressure/drug effects ; Corticosterone/administration & dosage ; Corticosterone/pharmacology ; Male ; Neuropeptide Y/metabolism ; Norepinephrine/metabolism ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; Rats, Sprague-Dawley ; Restraint, Physical/methods ; Rhombencephalon/drug effects ; Rhombencephalon/surgery ; Stress, Physiological ; Vasopressins/metabolism
    Chemical Substances Neuropeptide Y ; Proto-Oncogene Proteins c-fos ; Vasopressins (11000-17-2) ; Corticosterone (W980KJ009P) ; Norepinephrine (X4W3ENH1CV)
    Language English
    Publishing date 2014-05-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00326.2013
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Glucocorticoids reduce responses to AMPA receptor activation and blockade in nucleus tractus solitarius.

    Shank, Sylvan S / Scheuer, Deborah A

    American journal of physiology. Heart and circulatory physiology

    2003  Volume 284, Issue 5, Page(s) H1751–61

    Abstract: We tested the hypothesis that glucocorticoids attenuate changes in arterial pressure and renal sympathetic nerve activity (RSNA) in response to activation and blockade of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors within ... ...

    Abstract We tested the hypothesis that glucocorticoids attenuate changes in arterial pressure and renal sympathetic nerve activity (RSNA) in response to activation and blockade of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors within the nucleus of the solitary tract (NTS). Experiments were performed in Inactin-anesthetized male Sprague-Dawley rats treated for 7 +/- 1 days with a subcutaneous corticosterone (Cort) pellet or in control rats. Baseline mean arterial pressure (MAP) was significantly higher in Cort-treated rats (109 +/- 2 mmHg, n = 39) than in control rats (101 +/- 1 mmHg, n = 48, P < 0.05). In control rats, microinjection of AMPA (0.03, 0.1, and 0.3 pmol/100 nl) into the NTS significantly decreased MAP at all doses and decreased RSNA at 0.1 and 0.3 pmol/100 nl. Responses to AMPA in Cort-treated rats were attenuated at all doses of AMPA (P < 0.05). Responses to the AMPA-kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were also significantly reduced in Cort-treated rats relative to control rats. Blockade of glucocorticoid type II receptors with mifepristone significantly enhanced responses to CNQX in both control and Cort rats. We conclude that glucocorticoids attenuate MAP and RSNA responses to activation and blockade of AMPA receptors in the NTS.
    MeSH term(s) 2-Amino-5-phosphonovalerate/pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Anti-Inflammatory Agents/pharmacology ; Baroreflex/drug effects ; Corticosterone/pharmacology ; Drug Interactions ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/metabolism ; Hormone Antagonists/pharmacology ; Male ; Microinjections ; Mifepristone/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/antagonists & inhibitors ; Receptors, AMPA/metabolism ; Solitary Nucleus/drug effects ; Solitary Nucleus/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Excitatory Amino Acid Antagonists ; Hormone Antagonists ; Receptors, AMPA ; Mifepristone (320T6RNW1F) ; Glutamic Acid (3KX376GY7L) ; 6-Cyano-7-nitroquinoxaline-2,3-dione (6OTE87SCCW) ; 2-Amino-5-phosphonovalerate (76726-92-6) ; Corticosterone (W980KJ009P)
    Language English
    Publishing date 2003-01-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.01033.2002
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top