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Article ; Online: Blunted hypothalamo-pituitary adrenal axis response to predator odor predicts high stress reactivity.

Whitaker, Annie M / Gilpin, Nicholas W

2015 Volume 147, Page(s) 16–22

Abstract: Individuals with trauma- and stress-related disorders exhibit increases in avoidance of trauma-related stimuli, heightened anxiety and altered neuroendocrine stress responses. Our laboratory uses a rodent model of stress that mimics the avoidance symptom ...

Abstract	Individuals with trauma- and stress-related disorders exhibit increases in avoidance of trauma-related stimuli, heightened anxiety and altered neuroendocrine stress responses. Our laboratory uses a rodent model of stress that mimics the avoidance symptom cluster associated with stress-related disorders. Animals are classified as 'Avoiders' or 'Non-Avoiders' post-stress based on avoidance of predator-odor paired context. Utilizing this model, we are able to examine subpopulation differences in stress reactivity. Here, we used this predator odor model of stress to examine differences in anxiety-like behavior and hypothalamo-pituitary adrenal (HPA) axis function in animals that avoid a predator-paired context relative to those that do not. Rats were exposed to predator odor stress paired with a context and tested for avoidance (24h and 11days), anxiety-like behavior (48h and 5days) and HPA activation following stress. Control animals were exposed to room air. Predator odor stress produced avoidance in approximately 65% of the animals at 24h that persisted 11days post-stress. Both Avoiders and Non-Avoiders exhibited a heightened anxiety-like behavior at 48h and 5days post-stress when compared to unstressed Controls. Non-Avoiders exhibited significant increases in circulating adrenocorticotropin hormone (ACTH) and corticosterone (CORT) concentrations immediately following predator odor stress compared to Controls and this response was significantly attenuated in Avoiders. There was an inverse correlation between circulating ACTH/CORT concentrations and avoidance, indicating that lower levels of ACTH/CORT predicted higher levels of avoidance. These results suggest that stress effects on HPA stress axis activation predict long-term avoidance of stress-paired stimuli, and build on previous data showing the utility of this model for exploring the neurobiological mechanisms of trauma- and stress-related disorders.
MeSH term(s)	Adrenocorticotropic Hormone ; Analysis of Variance ; Animals ; Anxiety/blood ; Anxiety/etiology ; Anxiety/pathology ; Avoidance Learning/physiology ; Brain/pathology ; Conditioning, Operant ; Corticosterone ; Disease Models, Animal ; Exploratory Behavior ; Hypothalamo-Hypophyseal System/physiology ; Male ; Maze Learning ; Odorants ; Pituitary-Adrenal System/physiology ; Radioimmunoassay ; Rats ; Rats, Wistar ; Stress, Psychological/complications ; Stress, Psychological/etiology ; Time Factors
Chemical Substances	Adrenocorticotropic Hormone (9002-60-2) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2015-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2015.03.033
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Article ; Online: Angiotensin (1-7) contributes to nitric oxide tonic inhibition of vasopressin release during hemorrhagic shock in acute ethanol intoxicated rodents.

Whitaker, Annie M / Molina, Patricia E

Life sciences

2013 Volume 93, Issue 17, Page(s) 623–629

Abstract: Aims: Acute ethanol intoxication (AEI) attenuates the arginine vasopressin (AVP) response to hemorrhage leading to impaired hemodynamic counter-regulation and accentuated hemodynamic stability. Previously we identified that the ethanol-induced ... ...

Abstract	Aims: Acute ethanol intoxication (AEI) attenuates the arginine vasopressin (AVP) response to hemorrhage leading to impaired hemodynamic counter-regulation and accentuated hemodynamic stability. Previously we identified that the ethanol-induced impairment of circulating AVP concentrations in response to hemorrhage was the result of augmented central nitric oxide (NO) inhibition. The aim of the current study was to examine the mechanisms underlying ethanol-induced up-regulation of paraventricular nucleus (PVN) NO concentration. Angiotensin (ANG) (1-7) is an important mediator of NO production through activation of the Mas receptor. We hypothesized that Mas receptor inhibition would decrease central NO concentration and thus restore the rise in circulating AVP levels during hemorrhagic shock in AEI rats. Main methods: Conscious male Sprague-Dawley rats (300-325 g) received a 15 h intra-gastric infusion of ethanol (2.5 g/kg+300 mg/kg/h) or dextrose prior to a fixed-pressure (~40 mm Hg) 60 min hemorrhage. The Mas receptor antagonist A-779 was injected through an intracerebroventricular (ICV) cannula 15 min prior to hemorrhage. Key findings: PVN NOS activity and NO were significantly higher in AEI compared to DEX-treated controls at the completion of hemorrhage. ICV A-779 administration decreased NOS activity and NO concentration, partially restoring the rise in circulating AVP level at completion of hemorrhage in AEI rats. Significance: These results suggest that Mas receptor activation contributes to the NO-mediated inhibitory tone of AVP release in the ethanol-intoxicated hemorrhaged host.
MeSH term(s)	Alcoholic Intoxication/blood ; Alcoholic Intoxication/complications ; Alcoholic Intoxication/metabolism ; Angiotensin I/pharmacology ; Angiotensin II/administration & dosage ; Angiotensin II/analogs & derivatives ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/blood ; Arginine Vasopressin/drug effects ; Enzyme Inhibitors/pharmacology ; Hemodynamics/drug effects ; Injections, Intraventricular ; Male ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Paraventricular Hypothalamic Nucleus/drug effects ; Paraventricular Hypothalamic Nucleus/metabolism ; Peptide Fragments/administration & dosage ; Peptide Fragments/pharmacology ; Proto-Oncogene Proteins/antagonists & inhibitors ; Rats ; Receptors, G-Protein-Coupled/antagonists & inhibitors ; Renin-Angiotensin System/drug effects ; Shock, Hemorrhagic/blood ; Shock, Hemorrhagic/classification ; Shock, Hemorrhagic/metabolism ; Up-Regulation
Chemical Substances	7-Ala-angiotensin (1-7) ; Enzyme Inhibitors ; Peptide Fragments ; Proto-Oncogene Proteins ; Receptors, G-Protein-Coupled ; proto-oncogene proteins c-mas-1 ; Angiotensin II (11128-99-7) ; Arginine Vasopressin (113-79-1) ; Nitric Oxide (31C4KY9ESH) ; Angiotensin I (9041-90-1) ; Nitric Oxide Synthase (EC 1.14.13.39) ; angiotensin I (1-7) (IJ3FUK8MOF)
Language	English
Publishing date	2013-08-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2013.08.020
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Article ; Online: Animal models of post-traumatic stress disorder and recent neurobiological insights.

Whitaker, Annie M / Gilpin, Nicholas W / Edwards, Scott

Behavioural pharmacology

2014 Volume 25, Issue 5-6, Page(s) 398–409

Abstract: Post-traumatic stress disorder (PTSD) is a complex psychiatric disorder characterized by the intrusive re-experiencing of past trauma, avoidant behavior, enhanced fear, and hyperarousal following a traumatic event in vulnerable populations. Preclinical ... ...

Abstract	Post-traumatic stress disorder (PTSD) is a complex psychiatric disorder characterized by the intrusive re-experiencing of past trauma, avoidant behavior, enhanced fear, and hyperarousal following a traumatic event in vulnerable populations. Preclinical animal models do not replicate the human condition in its entirety, but seek to mimic symptoms or endophenotypes associated with PTSD. Although many models of traumatic stress exist, few adequately capture the complex nature of the disorder and the observed individual variability in susceptibility of humans to PTSD. In addition, various types of stressors may produce different molecular neuroadaptations that likely contribute to the various behavioral disruptions produced by each model, although certain consistent neurobiological themes related to PTSD have emerged. For example, animal models report traumatic stress-induced and trauma reminder-induced alterations in neuronal activity in the amygdala and prefrontal cortex, in agreement with the human PTSD literature. Models have also provided a conceptual framework for the often-observed combination of PTSD and comorbid conditions such as alcohol use disorder. Future studies will continue to refine preclinical PTSD models in hope of capitalizing on their potential to deliver new and more efficacious treatments for PTSD and associated psychiatric disorders.
MeSH term(s)	Animals ; Brain/physiopathology ; Disease Models, Animal ; Humans ; Stress Disorders, Post-Traumatic/physiopathology
Language	English
Publishing date	2014-07-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1027374-8
ISSN	1473-5849 ; 0955-8810
ISSN (online)	1473-5849
ISSN	0955-8810
DOI	10.1097/FBP.0000000000000069
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Zs.A 2883: Show issues

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Article ; Online: Post-traumatic stress avoidance is attenuated by corticosterone and associated with brain levels of steroid receptor co-activator-1 in rats.

Whitaker, Annie M / Farooq, Muhammad A / Edwards, Scott / Gilpin, Nicholas W

Stress (Amsterdam, Netherlands)

2016 Volume 19, Issue 1, Page(s) 69–77

Abstract: Individuals with post-traumatic stress disorder (PTSD) avoid trauma-related stimuli and exhibit blunted hypothalamic-pituitary-adrenal (HPA) axis activation at the time of stress. Our rodent model of stress mimics the avoidance symptom cluster of PTSD. ... ...

Abstract	Individuals with post-traumatic stress disorder (PTSD) avoid trauma-related stimuli and exhibit blunted hypothalamic-pituitary-adrenal (HPA) axis activation at the time of stress. Our rodent model of stress mimics the avoidance symptom cluster of PTSD. Rats are classified as "Avoiders" or "Non-Avoiders" post-stress based on the avoidance of a predator-odor paired context. Previously, we found Avoiders exhibit an attenuated HPA stress response to predator odor. We hypothesized that corticosterone administration before stress would reduce the magnitude and incidence of stress-paired context avoidance. Furthermore, we also predicted that Avoiders would exhibit altered expression of glucocorticoid receptor (GR) signaling machinery elements, including steroid receptor co-activator (SRC)-1. Male Wistar rats (n = 16) were pretreated with corticosterone (25 mg/kg) or saline and exposed to predator-odor stress paired with a context and tested for avoidance 24 h later. A second group of corticosterone-naïve rats (n = 24) were stressed (or not), indexed for avoidance 24 h later, and killed 48 h post-odor exposure to measure phosphorylated GR, FKBP51 and SRC-1 levels in the paraventricular nucleus (PVN), central amygdala (CeA) and ventral hippocampus (VH), all brain sites that highly express GRs and regulate HPA function. Corticosterone pretreatment reduced the magnitude and incidence of avoidance. In Avoiders, predator-odor exposure led to lower SRC-1 expression in the PVN and CeA, and higher SRC-1 expression in the VH. SRC-1 expression in PVN, CeA and VH was predicted by prior avoidance behavior. Hence, a blunted HPA stress response may contribute to stress-induced neuroadaptations in central SRC-1 levels and behavioral dysfunction in Avoider rats.
MeSH term(s)	Amygdala/metabolism ; Animals ; Avoidance Learning/drug effects ; Avoidance Learning/physiology ; Behavior, Animal/drug effects ; Behavior, Animal/physiology ; Brain/metabolism ; Corticosterone/pharmacology ; Hippocampus/metabolism ; Hypothalamo-Hypophyseal System/physiopathology ; Male ; Nuclear Receptor Coactivator 1/metabolism ; Paraventricular Hypothalamic Nucleus/metabolism ; Pituitary-Adrenal System/physiopathology ; Rats ; Rats, Wistar ; Receptors, Glucocorticoid/metabolism ; Stress Disorders, Post-Traumatic/physiopathology ; Stress, Psychological/metabolism ; Stress, Psychological/physiopathology ; Tacrolimus Binding Proteins/metabolism
Chemical Substances	NR3C1 protein, rat ; Receptors, Glucocorticoid ; Nuclear Receptor Coactivator 1 (EC 2.3.1.48) ; Tacrolimus Binding Proteins (EC 5.2.1.-) ; tacrolimus binding protein 5 (EC 5.2.1.8) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2016
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1387706-9
ISSN	1607-8888 ; 1025-3890
ISSN (online)	1607-8888
ISSN	1025-3890
DOI	10.3109/10253890.2015.1094689
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Zs.A 5673: Show issues

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Article: Angiotensin (1-7) contributes to nitric oxide tonic inhibition of vasopressin release during hemorrhagic shock in acute ethanol intoxicated rodents

Whitaker, Annie M / Molina, Patricia E

Life sciences. 2013 Oct. 17, v. 93, no. 17

2013

Abstract: AIMS: Acute ethanol intoxication (AEI) attenuates the arginine vasopressin (AVP) response to hemorrhage leading to impaired hemodynamic counter-regulation and accentuated hemodynamic stability. Previously we identified that the ethanol-induced impairment ...

Abstract	AIMS: Acute ethanol intoxication (AEI) attenuates the arginine vasopressin (AVP) response to hemorrhage leading to impaired hemodynamic counter-regulation and accentuated hemodynamic stability. Previously we identified that the ethanol-induced impairment of circulating AVP concentrations in response to hemorrhage was the result of augmented central nitric oxide (NO) inhibition. The aim of the current study was to examine the mechanisms underlying ethanol-induced up-regulation of paraventricular nucleus (PVN) NO concentration. Angiotensin (ANG) (1-7) is an important mediator of NO production through activation of the Mas receptor. We hypothesized that Mas receptor inhibition would decrease central NO concentration and thus restore the rise in circulating AVP levels during hemorrhagic shock in AEI rats. MAIN METHODS: Conscious male Sprague–Dawley rats (300–325g) received a 15h intra-gastric infusion of ethanol (2.5g/kg+300mg/kg/h) or dextrose prior to a fixed-pressure (~40mmHg) 60min hemorrhage. The Mas receptor antagonist A-779 was injected through an intracerebroventricular (ICV) cannula 15min prior to hemorrhage. KEY FINDINGS: PVN NOS activity and NO were significantly higher in AEI compared to DEX-treated controls at the completion of hemorrhage. ICV A-779 administration decreased NOS activity and NO concentration, partially restoring the rise in circulating AVP level at completion of hemorrhage in AEI rats. SIGNIFICANCE: These results suggest that Mas receptor activation contributes to the NO-mediated inhibitory tone of AVP release in the ethanol-intoxicated hemorrhaged host.
Keywords	antagonists ; arginine vasopressin ; ethanol ; glucose ; hemorrhage ; nitric oxide ; poisoning ; rats
Language	English
Dates of publication	2013-1017
Size	p. 623-629.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2013.08.020
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Alcohol abuse and the injured host: dysregulation of counterregulatory mechanisms review.

Molina, Patricia E / Sulzer, Jesse K / Whitaker, Annie M

Shock (Augusta, Ga.)

2013 Volume 39, Issue 3, Page(s) 240–249

Abstract: Traumatic injury ranks as the number one cause of death for the younger than 44 years age group and fifth leading cause of death overall (www.nationaltraumainstitute.org/home/trauma_statistics.html). Although improved resuscitation of trauma patients has ...

Abstract	Traumatic injury ranks as the number one cause of death for the younger than 44 years age group and fifth leading cause of death overall (www.nationaltraumainstitute.org/home/trauma_statistics.html). Although improved resuscitation of trauma patients has dramatically reduced immediate mortality from hemorrhagic shock, long-term morbidity and mortality continue to be unacceptably high during the postresuscitation period particularly as a result of impaired host immune responses to subsequent challenges such as surgery or infection. Acute alcohol intoxication (AAI) is a significant risk factor for traumatic injury, with intoxicating blood alcohol levels present in more than 40% of injured patients. Severity of trauma, hemorrhagic shock, and injury is higher in intoxicated individuals than that of sober victims, resulting in higher mortality rates in this patient population. Necessary invasive procedures (surgery, anesthesia) and subsequent challenges (infection) that intoxicated trauma victims are frequently subjected to are additional stresses to an already compromised inflammatory and neuroendocrine milieu and further contribute to their morbidity and mortality. Thus, dissecting the dynamic imbalance produced by AAI during trauma is of critical relevance for a significant proportion of injured victims. This review outlines how AAI at the time of hemorrhagic shock not only prevents adequate responses to fluid resuscitation but also impairs the ability of the host to overcome a secondary infection. Moreover, it discusses the neuroendocrine mechanisms underlying alcohol-induced hemodynamic dysregulation and its relevance to host defense restoration of homeostasis after injury.
MeSH term(s)	Alcoholism/complications ; Alcoholism/physiopathology ; Autonomic Nervous System/physiopathology ; Ethanol/poisoning ; Hemodynamics/physiology ; Humans ; Neurophysins/physiology ; Neurosecretory Systems/physiopathology ; Protein Precursors/physiology ; Resuscitation/methods ; Shock, Hemorrhagic/etiology ; Shock, Hemorrhagic/physiopathology ; Shock, Hemorrhagic/therapy ; Vasopressins/physiology ; Wounds and Injuries/etiology ; Wounds and Injuries/physiopathology
Chemical Substances	AVP protein, human ; Neurophysins ; Protein Precursors ; Vasopressins (11000-17-2) ; Ethanol (3K9958V90M)
Language	English
Publishing date	2013-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0b013e318285b86d
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Zs.A 3985: Show issues

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Article: Evaluating Demographic Representation in Clinical Trials: Use of the Adaptive Coronavirus Disease 2019 Treatment Trial (ACTT) as a Test Case.

Ortega-Villa, Ana M / Hynes, Noreen A / Levine, Corri B / Yang, Katherine / Wiley, Zanthia / Jilg, Nikolaus / Wang, Jing / Whitaker, Jennifer A / Colombo, Christopher J / Nayak, Seema U / Kim, Hannah Jang / Iovine, Nicole M / Ince, Dilek / Cohen, Stuart H / Langer, Adam J / Wortham, Jonathan M / Atmar, Robert L / El Sahly, Hana M / Jain, Mamta K /

Open forum infectious diseases

2023 Volume 10, Issue 6, Page(s) ofad290

Abstract: Background: Clinical trials initiated during emerging infectious disease outbreaks must quickly enroll participants to identify treatments to reduce morbidity and mortality. This may be at odds with enrolling a representative study population, ... ...

Abstract	Background: Clinical trials initiated during emerging infectious disease outbreaks must quickly enroll participants to identify treatments to reduce morbidity and mortality. This may be at odds with enrolling a representative study population, especially when the population affected is undefined. Methods: We evaluated the utility of the Centers for Disease Control and Prevention's COVID-19-Associated Hospitalization Surveillance Network (COVID-NET), the COVID-19 Case Surveillance System (CCSS), and 2020 United States (US) Census data to determine demographic representation in the 4 stages of the Adaptive COVID-19 Treatment Trial (ACTT). We compared the cumulative proportion of participants by sex, race, ethnicity, and age enrolled at US ACTT sites, with respective 95% confidence intervals, to the reference data in forest plots. Results: US ACTT sites enrolled 3509 adults hospitalized with COVID-19. When compared with COVID-NET, ACTT enrolled a similar or higher proportion of Hispanic/Latino and White participants depending on the stage, and a similar proportion of African American participants in all stages. In contrast, ACTT enrolled a higher proportion of these groups when compared with US Census and CCSS. The proportion of participants aged ≥65 years was either similar or lower than COVID-NET and higher than CCSS and the US Census. The proportion of females enrolled in ACTT was lower than the proportion of females in the reference datasets. Conclusions: Although surveillance data of hospitalized cases may not be available early in an outbreak, they are a better comparator than US Census data and surveillance of all cases, which may not reflect the population affected and at higher risk of severe disease.
Language	English
Publishing date	2023-05-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2757767-3
ISSN	2328-8957
ISSN	2328-8957
DOI	10.1093/ofid/ofad290
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Article ; Online: Hypertonic saline resuscitation enhances blood pressure recovery and decreases organ injury following hemorrhage in acute alcohol intoxicated rodents.

Sulzer, Jesse K / Whitaker, Annie M / Molina, Patricia E

The journal of trauma and acute care surgery

2012 Volume 74, Issue 1, Page(s) 196–202

Abstract: Background: Acute alcohol intoxication (AAI) impairs the hemodynamic and arginine vasopressin (AVP) counter-regulation to hemorrhagic shock (HS) and lactated Ringer's solution (LR) fluid resuscitation (FR). The mechanism of AAI-induced suppression of ... ...

Abstract	Background: Acute alcohol intoxication (AAI) impairs the hemodynamic and arginine vasopressin (AVP) counter-regulation to hemorrhagic shock (HS) and lactated Ringer's solution (LR) fluid resuscitation (FR). The mechanism of AAI-induced suppression of AVP release in response to HS involves accentuated nitric oxide (NO) inhibitory tone. In contrast, AAI does not prevent AVP response to increased osmolarity produced by hypertonic saline (HTS) infusion. We hypothesized that FR with HTS during AAI would enhance AVP release by decreasing periventricular nucleus NO inhibitory tone, subsequently improving mean arterial blood pressure (MABP) and organ perfusion. Methods: Male Sprague-Dawley rats received a 15-hour alcohol infusion (2.5 g/kg + 0.3 g/kg/h) or dextrose (DEX) before HS (40 mm Hg × 60 minutes) and FR with HTS (7.5%, 4 ml/kg) or LR (2.4 × blood volume removed). Organ blood flow was determined, and brains were collected for NO content at 2 hours after FR. Results: HTS improved MABP recovery in AAI (109 vs. 80 mm Hg) and DEX (114 vs. 83 mm Hg) animals compared with LR. This was associated with higher (>60%) circulating AVP levels at 2 hours after FR compared with those detected in LR animals in both groups. Neither AAI alone nor HS in DEX animals resuscitated with LR altered organ blood flow. In AAI animals, HS and FR with LR reduced blood flow to the liver (72%), small intestine (65%), and large intestine (67%) compared with shams. FR with HTS improved liver (threefold) and small intestine (twofold) blood flow compared with LR in AAI-HS animals. The enhanced MABP response to HTS was prevented by pretreatment with a systemic AVP V1a receptor antagonist. HTS decreased periventricular nucleus NO content in both groups 2 hours after FR. Conclusion: These results suggest that FR with HTS in AAI results in the removal of central NO inhibition of AVP, restoring AVP levels and improving MABP and organ perfusion in AAI-HS.
MeSH term(s)	Alcoholic Intoxication/complications ; Alcoholic Intoxication/physiopathology ; Alcoholic Intoxication/therapy ; Animals ; Arginine Vasopressin/blood ; Blood Pressure ; Intestines/blood supply ; Isotonic Solutions ; Kidney/blood supply ; Liver/blood supply ; Male ; Nitric Oxide/blood ; Peroxidase/blood ; Rats ; Rats, Sprague-Dawley ; Regional Blood Flow ; Resuscitation ; Ringer's Lactate ; Saline Solution, Hypertonic/therapeutic use ; Shock, Hemorrhagic/complications ; Shock, Hemorrhagic/physiopathology ; Shock, Hemorrhagic/therapy
Chemical Substances	Isotonic Solutions ; Ringer's Lactate ; Saline Solution, Hypertonic ; Arginine Vasopressin (113-79-1) ; Nitric Oxide (31C4KY9ESH) ; Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2012-11-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2651070-4
ISSN	2163-0763 ; 2163-0755
ISSN (online)	2163-0763
ISSN	2163-0755
DOI	10.1097/TA.0b013e31826fc747
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Article ; Online: Resistance exercise lowers blood pressure and improves vascular endothelial function in individuals with elevated blood pressure or stage-1 hypertension.

Banks, Nile F / Rogers, Emily M / Stanhewicz, Anna E / Whitaker, Kara M / Jenkins, Nathaniel D M

American journal of physiology. Heart and circulatory physiology

2023 Volume 326, Issue 1, Page(s) H256–H269

Abstract: Lifestyle modifications are the first-line treatment recommendation for elevated blood pressure (BP) or stage-1 hypertension (E/S1H) and include resistance exercise training (RET). The purpose of the current study was to examine the effect of a 9-wk RET ... ...

Abstract	Lifestyle modifications are the first-line treatment recommendation for elevated blood pressure (BP) or stage-1 hypertension (E/S1H) and include resistance exercise training (RET). The purpose of the current study was to examine the effect of a 9-wk RET intervention in line with the current exercise guidelines for individuals with E/S1H on resting peripheral and central BP, vascular endothelial function, central arterial stiffness, autonomic function, and inflammation in middle-aged and older adults (MA/O) with untreated E/S1H. Twenty-six MA/O adults (54 ± 6 yr; 16 females/10 males) with E/S1H engaged in either 9 wk of 3 days/wk RET (
MeSH term(s)	Male ; Female ; Middle Aged ; Humans ; Aged ; Blood Pressure/physiology ; Resistance Training ; Pulse Wave Analysis ; Hypertension/therapy ; Exercise/physiology ; Vascular Stiffness/physiology
Language	English
Publishing date	2023-11-17
Publishing country	United States
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00386.2023
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Article ; Online: Augmented central nitric oxide production inhibits vasopressin release during hemorrhage in acute alcohol-intoxicated rodents.

Whitaker, Annie M / Sulzer, Jesse K / Molina, Patricia E

American journal of physiology. Regulatory, integrative and comparative physiology

2011 Volume 301, Issue 5, Page(s) R1529–39

Abstract: Acute alcohol intoxication (AAI) attenuates the AVP response to hemorrhage, contributing to impaired hemodynamic counter-regulation. This can be restored by central cholinergic stimulation, implicating disrupted signaling regulating AVP release. AVP is ... ...

Abstract	Acute alcohol intoxication (AAI) attenuates the AVP response to hemorrhage, contributing to impaired hemodynamic counter-regulation. This can be restored by central cholinergic stimulation, implicating disrupted signaling regulating AVP release. AVP is released in response to hemorrhage and hyperosmolality. Studies have demonstrated nitric oxide (NO) to play an inhibitory role on AVP release. AAI has been shown to increase NO content in the paraventricular nucleus. We hypothesized that the attenuated AVP response to hemorrhage during AAI is the result of increased central NO inhibition. In addition, we predicted that the increased NO tone during AAI would impair the AVP response to hyperosmolality. Conscious male Sprague-Dawley rats (300-325 g) received a 15-h intragastric infusion of alcohol (2.5 g/kg + 300 mg·kg(-1)·h(-1)) or dextrose prior to a 60-min fixed-pressure hemorrhage (∼40 mmHg) or 5% hypertonic saline infusion (0.05 ml·kg(-1)·min(-1)). AAI attenuated the AVP response to hemorrhage, which was associated with increased paraventricular NO content. In contrast, AAI did not impair the AVP response to hyperosmolality. This was accompanied by decreased paraventricular NO content. To confirm the role of NO in the alcohol-induced inhibition of AVP release during hemorrhage, the nitric oxide synthase inhibitor, nitro-l-arginine methyl ester (l-NAME; 250 μg/5 μl), was administered centrally prior to hemorrhage. l-NAME did not further increase AVP levels during hemorrhage in dextrose-treated animals; however, it restored the AVP response during AAI. These results indicate that AAI impairs the AVP response to hemorrhage, while not affecting the response to hyperosmolality. Furthermore, these data demonstrate that the attenuated AVP response to hemorrhage is the result of augmented central NO inhibition.
MeSH term(s)	Alcoholic Intoxication/blood ; Alcoholic Intoxication/complications ; Alcoholic Intoxication/metabolism ; Alcoholic Intoxication/physiopathology ; Animals ; Arginine Vasopressin/metabolism ; Blood Pressure ; Blood Volume ; Disease Models, Animal ; Down-Regulation ; Enzyme Inhibitors/pharmacology ; Hemorrhage/blood ; Hemorrhage/complications ; Hemorrhage/metabolism ; Hemorrhage/physiopathology ; Male ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/metabolism ; Osmolar Concentration ; Paraventricular Hypothalamic Nucleus/drug effects ; Paraventricular Hypothalamic Nucleus/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Supraoptic Nucleus/metabolism ; Time Factors ; Up-Regulation
Chemical Substances	Enzyme Inhibitors ; Arginine Vasopressin (113-79-1) ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2011-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00035.2011
Database	MEDical Literature Analysis and Retrieval System OnLINE

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