Publications by authors named "Milena Samora"

An exaggerated exercise pressor reflex and peripheral neuropathy are both evoked by the same type of thinly myelinated afferents and are present in patients with type 2 diabetes mellitus (T2DM). Although it is known that the pro-inflammatory cytokine interleukin-1β (IL-1β) contributes to peripheral neuropathy, the effects of IL-1β on the exercise pressor reflex in T2DM are not known. Therefore, we aimed to determine the effect of IL-1 receptors on the exercise pressor reflex in T2DM.

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Cyclooxygenase (COX) products of arachidonic acid metabolism, specifically prostaglandins, play a role in evoking and transmitting the exercise pressor reflex in health and disease. Individuals with type 2 diabetes mellitus (T2DM) have an exaggerated exercise pressor reflex; however, the mechanisms for this exaggerated reflex are not fully understood. We aimed to determine the role played by COX products in the exaggerated exercise pressor reflex in T2DM rats.

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Patients with type 2 diabetes mellitus (T2DM) have impaired arterial baroreflex function, which may be linked to the co-existence of obesity. However, the role of obesity and its related metabolic impairments on baroreflex dysfunction in T2DM is unknown. This study aimed to investigate the role of visceral fat and adiponectin, the most abundant cytokine produced by adipocytes, on baroreflex dysfunction in T2DM rats.

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Exaggerated cardiovascular responses to exercise increase the risk of myocardial infarction and stroke in individuals with type 1 diabetes (T1D); however, the underlying mechanisms remain largely elusive. This review provides an overview of the altered exercise pressor reflex in T1D, with an emphasis on the mechanical component of the reflex.

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Studies in humans and animals have found that type 2 diabetes mellitus (T2DM) exaggerates the blood pressure (BP) response to exercise, which increases the risk of adverse cardiovascular events such as heart attack and stroke. T2DM is a chronic disease that, without appropriate management, progresses in severity as individuals grow older. Thus, it is possible that aging may also exaggerate the BP response to exercise.

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Resting beat-to-beat blood pressure variability is a powerful predictor of cardiovascular events and end-organ damage. However, its underlying mechanisms remain unknown. Herein, we tested the hypothesis that a potentiation of GABAergic synaptic transmission by diazepam would acutely increase resting beat-to-beat blood pressure variability.

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Fluctuations in diastolic pressure modulate muscle sympathetic nerve activity (MSNA) through the arterial baroreflex. A higher sympathetic baroreflex sensitivity (sBRS) to pressure falls compared with rises has been reported; however, the underlying mechanisms are unclear. We assessed whether beat-to-beat falling and rising diastolic pressures operate on two distinct baroreflex response curves.

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A parasympathetic reactivation is an underlying mechanism mediating the rapid fall in heart rate (HR) at the onset of post-exercise ischemia (PEI) in humans. Herein, we tested the hypothesis that, compared to men, women present a slower HR recovery at the cessation of isometric handgrip exercise (i.e.

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Cerebral blood flow is tightly coupled with local neuronal activation and metabolism, i.e., neurovascular coupling (NVC).

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The arterial baroreflex has dominant control over multiunit muscle sympathetic nerve activity (MSNA) burst occurrence, but whether this extends to all single units or is influenced by resting blood pressure status is unclear. In 22 men (32 ± 8 yr), we assessed 68 MSNA single units during sequential bolus injections of nitroprusside and phenylephrine (modified Oxford). Sympathetic baroreflex sensitivity (sBRS) was quantified as the weighted negative linear regression slope between diastolic blood pressure (DBP) and single-unit spike firing probability and multiple spike firing.

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We sought to investigate whether the β-adrenergic receptors play a pivotal role in sex-related differences in arterial blood pressure (BP) regulation during isometric exercise. Sixteen volunteers (8 women) performed 2 min of ischemic isometric handgrip exercise (IHE) and 2 min of postexercise circulatory occlusion (PECO). Heart rate (HR) and beat-to-beat arterial BP were continuously measured.

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New Findings: What is the central question of this study? The initial circulatory response to isometric exercise in young healthy subjects is thought to be cholinergically mediated. Do patients with Parkinson's disease, a specific population known to present cholinergic dysfunction, present impairment in these initial circulatory responses? What is the main finding and its importance? The initial reduction in total peripheral resistance was absent in patients with Parkinson's disease and in older subjects, which augmented the pressor response at the onset of isometric handgrip exercise. Given that cholinergic mechanisms play an important role in the circulatory responses at the onset of isometric exercise in humans, our data suggest that cholinergic mechanisms might be compromised with ageing.

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The cardiovascular responses to exercise are mediated by several interactive neural mechanisms, including central command, arterial baroreflex, and skeletal muscle mechano- and metaboreflex. In humans, muscle metaboreflex activation can be isolated via postexercise ischemia (PEI), which increases sympathetic nerve activity and partially maintains the exercise-induced increase in arterial blood pressure. Here, we describe a practical laboratory class using PEI as a simple and useful technique to teach cardiovascular physiology.

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Purpose: To investigate the effect of isolated muscle metaboreflex activation on spontaneous cardiac baroreflex sensitivity (cBRS), and to characterize the potential sex-related differences in this interaction in young healthy subjects.

Methods: 40 volunteers (20 men and 20 women, age: 22 ± 0.4 year) were recruited.

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Patients with Parkinson's disease (PD) exhibit attenuated cardiovascular responses to exercise. The underlying mechanisms that are potentially contributing to these impairments are not fully understood. Therefore, we sought to test the hypothesis that patients with PD exhibit blunted cardiovascular responses to isolated muscle metaboreflex activation following exercise.

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Previous studies have indicated that central GABAergic mechanisms are involved in the heart rate (HR) responses at the onset of exercise. On the basis of previous research that showed similar increases in HR during passive and active cycling, we reasoned that the GABAergic mechanisms involved in the HR responses at the exercise onset are primarily mediated by muscle mechanoreceptor afferents. Therefore, in this study, we sought to determine whether central GABA mechanisms are involved in the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans.

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