Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex

Resstel, Leonardo Barbosa Moraes; Corrêa, Fernando Morgan de Aguiar

doi:10.1111/j.1460-9568.2005.04566.x

Cited by 49 publications

(40 citation statements)

References 54 publications

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“…Increased sympathoadrenal tone 21 with subsequent release of renin and vasoconstriction of arterioles results from (1) direct injury to inhibitory or modulatory brain regions or (2) indirect effects of reduced parasympathetic activity, 22 which leads to impaired cardiac baroreceptor sensitivity in patients with stroke. 23 Although direct injury is the most likely explanation, an indirect effect of muscle paralysis 24 or the release of neurotransmitters such as nitric oxide 25 during ischemia may be contributing factors to altered activity of these nuclei. Other stress responses to hospitalization, headache, urinary retention, or concomitant infection 26 may lead to abnormal autonomic activity and raised levels of circulating catecholamines 27 and inflammatory cytokines 12 and subsequently may contribute to the hypertensive response.…”

Section: Underlying Causes Of Acute Hypertensive Responsementioning

confidence: 99%

Acute Hypertensive Response in Patients With Stroke

2008

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A cute hypertensive response is the elevation of blood pressure (BP) above normal and premorbid values that initially occurs within the first 24 hours of symptom onset in patients with stroke. This phenomenon was reported in Ͼ60% of patients presenting with stroke in a nationally representative study from the United States. 1 With Ϸ980 000 patients 2 admitted with stroke each year in the United States, the estimated annual prevalence of acute hypertensive response is more than half a million patients. With Ϸ15 million patients experiencing stroke worldwide each year, 3 the acute hypertensive response may be expected in Ϸ10 million patients per year. The acute hypertensive response in stroke patients is managed by a diverse group of physicians, including emergency physicians, intensivists, internists, primary care physicians, neurologists, neurosurgeons, and cardiologists. Previous audits suggest that antihypertensive agents and management strategies vary considerably and are not always consistent with recommended guidelines. 4 Data from 1181 acute ischemic stroke patients enrolled in the Project for Improvement of Stroke Care Management suggested that administration of antihypertensive medication within 24 hours in 56% of the patients was inconsistent with guidelines provided by the American Stroke Association (ASA). 5 The present review article summarizes the current concepts pertaining to treatment of the acute hypertensive response derived from recent guidelines provided by professional organizations and "best available" evidence derived from experimental and clinical studies and discusses incorporation of these concepts into clinical practice. Randomized trials, nonrandomized controlled studies, and selected observational studies were identified with multiple searches on Medline from 1980 to 2007 by cross-referencing the key words of stroke, acute hypertension, antihypertensive agents, acute stroke, and hypertension. Pertinent articles identified from bibliographies of selected articles were also reviewed. Treatment targets and strategies were identified by review of existing guidelines from professional organizations. Definition of Acute Hypertensive ResponseThe 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement 6 and the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) 7 define hypertension on the basis of the presence of consistent BP Ն140/90 mm Hg (multiple readings on separate days). This definition of hypertension is a threshold for the use of long-term antihypertensive treatment that is supported by evidence derived from randomized trials and clinicor population-based data that demonstrate reduction in cardiovascular events with this threshold for treatment. The same definition cannot be applied in the case of acute hypertensive response, because the above-mentioned ascertainment criteria and rationale are not valid. The executive summary of the ISH statement 8 on management of BP i...

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Section: Underlying Causes Of Acute Hypertensive Responsementioning

confidence: 99%

Acute Hypertensive Response in Patients With Stroke

2008

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“…50 The defensive responses elicited by the CS in animals are characterized by freezing (complete immobility except as required for breathing), reflex expression (characterized by fear-potentiated startle), and autonomic (increase in heart rate and in the mean arterial pressure) and endocrine (stress-related hormone release) responses. [50][51][52][53] Fear conditioning models involve the encoding of traumatic memories, representing a psychological stress without physical stimuli. 51,54 They have been associated with a vulnerability to phobic fears and other anxiety-related disorders, such as panic disorder (PD), agoraphobia, and posttraumatic stress disorder (PTSD).…”

Section: Fear Conditioningmentioning

confidence: 99%

Animal models of anxiety disorders and stress

Campos

Fogaça

Aguiar

et al. 2013

Rev. Bras. Psiquiatr.

365

246

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Anxiety and stress-related disorders are severe psychiatric conditions that affect performance in daily tasks and represent a high cost to public health. The initial observation of Charles Darwin that animals and human beings share similar characteristics in the expression of emotion raise the possibility of studying the mechanisms of psychiatric disorders in other mammals (mainly rodents). The development of animal models of anxiety and stress has helped to identify the pharmacological mechanisms and potential clinical effects of several drugs. Animal models of anxiety are based on conflict situations that can generate opposite motivational states induced by approach-avoidance situations. The present review revisited the main rodent models of anxiety and stress responses used worldwide. Here we defined as ''ethological'' the tests that assess unlearned/unpunished responses (such as the elevated plus maze, light-dark box, and open field), whereas models that involve learned/ punished responses are referred to as ''conditioned operant conflict tests'' (such as the Vogel conflict test). We also discussed models that involve mainly classical conditioning tests (fear conditioning). Finally, we addressed the main protocols used to induce stress responses in rodents, including psychosocial (social defeat and neonatal isolation stress), physical (restraint stress), and chronic unpredictable stress.

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“…Furthermore, a previous study from our group showed that local injection of L-glutamate into the vMPFC evokes an activation of both sympathetic and parasympathetic activities on the heart of unanesthetized rats (48). Moreover, the glutamatergic system present in the vMPFC is involved in baroreflex modulation (45).…”

mentioning

confidence: 99%

Medial prefrontal cortex endocannabinoid system modulates baroreflex activity through CB₁receptors

Ferreira‐Junior

Fedoce

Alves

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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[481][482][483][484][485][486][487][488] 2006) have shown that glutamatergic synapses in the ventral portion of the medial prefrontal cortex (vMPFC) modulate baroreflex activity. Moreover, glutamatergic neurotransmission in the vMPFC can be modulated by the endocannabinoids system (eCBs), particularly the endocannabinoid anandamide, through presynaptic CB 1 receptor activation. Therefore, in the present study, we investigated eCBs receptors that are present in the vMPFC, and more specifically whether CB1 receptors modulate baroreflex activity. We found that bilateral microinjection of the CB 1 receptor antagonist AM251 (100 or 300 pmol/200 nl) into the vMPFC increased baroreflex activity in unanesthetized rats. Moreover, bilateral microinjection of either the anandamide transporter inhibitor AM404 (100 pmol/200 nl) or the inhibitor of the enzyme fatty acid amide hydrolase that degrades anandamide, URB597 (100 pmol/200 nl), into the MPFC decreased baroreflex activity. Finally, pretreatment of the vMPFC with an ineffective dose of AM251 (10 pmol/200 nl) was able to block baroreflex effects of both AM404 and URB597. Taken together, our results support the view that the eCBs in the vMPFC is involved in the modulation of baroreflex activity through the activation of CB1 receptors, which modulate local glutamate release.anandamide; autonomic system; cannabinoids; infralimbic cortex; prelimbic cortex THE MEDIAL PREFRONTAL CORTEX (MPFC) is a limbic structure that is involved in the modulation of autonomic responses exerting influence on the cardiovascular system in rats (44, 57). The ventral portion of the MPFC (vMPFC), which is compounded by the infralimbic (IL), prelimbic (PL), and dorsal peduncular cortexes (41, 61), is involved in the modulation of baroreflex activity (49,56).Glutamatergic terminals and ionotropic glutamate receptors were reported in the vMPFC of rats (18,36). Furthermore, a previous study from our group showed that local injection of L-glutamate into the vMPFC evokes an activation of both sympathetic and parasympathetic activities on the heart of unanesthetized rats (48). Moreover, the glutamatergic system present in the vMPFC is involved in baroreflex modulation (45).In the central nervous system (CNS), the endocannabinoid anandamide is synthesized on demand in postsynaptic neurons, after calcium influx increase (13,42). Anandamide immediately diffuses to the synaptic cleft, activating CB 1 cannabinoid receptors, which are located in presynaptic terminals (59). The action of anandamide is limited by its reuptake through a putative anandamide transporter, being subsequently metabolized by the intracellular enzyme fatty acid amide hydrolase (FAAH) that is located in postsynaptic neurons (14, 43). These two mechanisms, which cooperate to attenuate anandamide signaling in the CNS, can be pharmacologically inhibited by drugs such as AM404 (anandamide re-uptake inhibitor) and URB597 (FAAH inhibitor).The CB 1 cannabinoid receptor is one of the most abundant G protein-coupled receptors in the brain and ...

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Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex

Cited by 49 publications

References 54 publications

Acute Hypertensive Response in Patients With Stroke

Acute Hypertensive Response in Patients With Stroke

Animal models of anxiety disorders and stress

Medial prefrontal cortex endocannabinoid system modulates baroreflex activity through CB₁receptors

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Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex

Cited by 49 publications

References 54 publications

Acute Hypertensive Response in Patients With Stroke

Acute Hypertensive Response in Patients With Stroke

Animal models of anxiety disorders and stress

Medial prefrontal cortex endocannabinoid system modulates baroreflex activity through CB1receptors

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Product

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Medial prefrontal cortex endocannabinoid system modulates baroreflex activity through CB₁receptors