Browsing by Subject "Blood Pressure"
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Item Interaction of the Exercise Pressor Reflex with Central Command in the Regulation of Blood Pressure During Dynamic Exercise(1996-12-01) Smith, Scott Alan; Peter B. Raven; Patricia A. GwirtzSmith, Scott A., Interaction of the exercise pressor reflex with central command in the regulation of blood pressure during dynamic exercise. Master of Science (Biomedical Sciences, Integrative Physiology), October, 1996, 73 pp., 7 tables, 8 figures, references. Ten subjects, aged 26.5±3.7 years, performed incremental workload cycling exercise to investigate the interaction of skeletal muscle mechano- and metaboreceptors in the regulation of blood pressure. Each subject performed four bouts of exercise: control (exercise with no intervention); exercise with thigh cuff inflation to 90 mmHg (to reduce venous outflow stimulating metaboreceptors); exercise with application of lower body positive pressure (LBPP) to 45 mmHg (to enhance mechanoreceptor activation); and exercise with application of lower body positive pressure (LBPP) to 45 mmHg (to enhance mechanoreceptor activation); and exercise with the application of both LBPP and thigh cuff inflation. Measurements of mean arterial pressure (MAP), heart rate (HR), electromyographic activity (EMG), rate of oxygen uptake (VO2)3 cardiac output (Q), and rating of perceived exertion for both the body (RPEB) and the legs (RPEL) were monitored. Significant mean data is presented. Indices of central command (HR, EMG, and VO2) were not significantly different between the four bouts of exercise indicating that the blood pressure response to central command activity was not altered by the interventions. Significant changes in RPEL from control during inflation of thigh cuffs, application of LBPP, and their combination indicate these stimuli successfully enhanced mechano- and metaboreceptor activation. Results indicate that MAP was significantly elevated from control only with the application of LBPP or the combination of LBPP and thigh cuff inflation. These data suggest that mechanoreceptors are the primary exercise pressor mediator of arterial blood pressure during submaximal dynamic exercise.Item Investigating the Use of Resistance Breathing for the Detection of Acute Hypovolemia(2021-05) Rusy, Ryan; Rickards, Caroline A.; Goulopoulou, Styliani; Mallet, Robert T.; Olivencia-Yurvati, Albert H.Introduction: Standard vital signs (e.g., heart rate and blood pressure) lack sensitivity and specificity to detect blood volume status following hemorrhage. Inspiratory resistance breathing has therapeutic potential to increase blood pressure and cardiac output following blood loss. We investigated the potential utility of resistance breathing as a novel method to detect volume loss. We hypothesized that resistance breathing would elicit greater increases in absolute and breath-to-breath amplitude of stroke volume and arterial pressure under hypovolemic vs. normovolemic conditions. Methods: Data were retrospectively analyzed from 23 healthy human subjects aged 23-40 years. Subjects underwent lower body negative pressure (LBNP) protocols to simulate hemorrhage with and without resistance breathing (via an impedance threshold device, ITD). Continuous arterial pressure and stroke volume were measured via finger photoplethysmography. Comparisons of absolute and changes in the breath-to-breath amplitude of arterial pressure and stroke volume were made under 4 conditions: 1) normovolemia; 2) normovolemia + resistance breathing; 3) hypovolemia, and; 4) hypovolemia + resistance breathing. The sensitivity and specificity of breath-to-breath arterial pressure and stroke volume amplitude responses in distinguishing between normovolemia and hypovolemia were assessed via area under the curve (AUC) of receiver operating characteristic (ROC) curves. Results: With resistance breathing the amplitude of systolic arterial pressure (P=0.007), diastolic arterial pressure (P<0.001), and mean arterial pressure (P<0.001) increased during hypovolemia vs. normovolemia, and the amplitude of stroke volume decreased (P=0.002). In distinguishing between normovolemia and hypovolemia, the ROC AUC were >0.86 for breath-by-breath mean, maximum and minimum stroke volume responses, and 0.77 for the amplitude response. The ROC AUC for mean arterial pressure amplitude was 0.88, and 0.64, 0.54, and 0.72 for the mean, maximum and minimum responses. Conclusions: The dynamic responses of arterial pressure and stroke volume with resistance breathing during hypovolemia show promise as a diagnostic tool for detection of hypovolemia in humans.Item Synergy 2011: Annual Research Report(2011-01-01)Item The Phenotype of Cells Expressing Estrogen Receptor Alpha in the Nucleus of the Solitary Tract(2018-05) Horn, Christopher L.; Mifflin, Steve W.; Schreihofer, Ann M.; Cunningham, J. Thomas; Phillips, Nicole R.Estrogen protects females from hypertension. The nucleus tractus solitarius (NTS) is a hindbrain site involved in the regulation of blood pressure, however little is known about estrogen receptors within the NTS. The purpose of these studies was to determine the phenotype of the cells expressing estrogen alpha receptors in the nucleus tractus solitarius. Four female Sprague-Dawley rats were transcardially perfused with 4% paraformaldehyde and hindbrains harvested. In coronal sections containing the NTS (40μm thick), immunohistochemistry was performed to determine which type of cells were expressed with estrogen receptor alpha (ERα) expressing cells. We used the anti-ERα antibody with an antibody for each protein of interest: anti-tyrosine hydroxylase (TH), anti-glial fibrillary acidic protein (GFAP), anti-NeuN, and anti-Iba-1. Sections were captured using an Olympus BX41 Fluorescence Microscope and analyzed using ImageJ. The NTS was divided into 2 regions: sections caudal to the area postrema (caudal) and sections lying below the area postrema (sub-postrema, SP) and the number of immunoreactive neurons in each region counted and expressed as an average number of labeled neurons per section±SEM. The number of sections analyzed ranged from 5-10 per individual in caudal and 2-4 per individual in SP. At sacrifice, females were in estrus (1), diestrus (2) or proestrus (3). NeuN in SP NTS (n=4) was observed in 151±53 and ERα in 50±21 neurons per section. Colocalization of ERα and NeuN in SP NTS was observed in 11±6 neurons per section (about 7%). NeuN in caudal NTS was observed in 59±7 and ERα 27±3 neurons per section. Colocalization of ERα and NeuN in caudal NTS was observed in 4±1 neurons per section (about 7%). TH in SP NTS (n=6) was observed in 49±8 and ERα in 51±12 neurons per section. Colocalization of ERα and TH in SP NTS was observed in 26±4 neurons per section (about 53%). TH in caudal NTS was observed in 26±6 and ERα 29±7 neurons per section. Colocalization of ERα and TH in caudal NTS was observed in 17±4 neurons per section (about 51%). Due to the quantity and shape of GFAP immunoreactive cells in the NTS (n=4), we were not able to count the number cells. Colocalization of ERα and GFAP expressing cells were not observed in our study. Cells expressing Iba1 were not observed in the later trials of our study (n=4). ERα is expressed on a subset of catecholaminergic NTS neurons, as well as non-catecholaminergic neurons. Since the NTS catecholaminergic neurons contribute to responses to stress (e.g., hypoxia), this finding could provide a substrate for estrogen-mediated cardiovascular protection in females.Item The Role of the MnPO in Body Fluid Balance and Blood Pressure Regulation(2019-05) Marciante, Alexandria B.; Cunningham, J. Thomas; Mifflin, Steve W.; Schreihofer, Ann M.; Goulopoulou, Styliani; Ma, Rong; Bugnariu, Nicoleta L.The median preoptic nucleus (MnPO) is situated on the anteroventral wall of the third ventricle (AV3V) between two circumventricular organs (CVOs) that lack a functional blood-brain barrier, the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT). The SFO and OVLT project to the MnPO and together these regions regulate neuroendocrine and autonomic function, arousal, and fluid balance. Early studies demonstrated that the MnPO and other regions in the AV3V contribute to regulating thirst associated with body fluid homeostasis, as well as several forms of neurogenic hypertension. The MnPO is key in relaying signals from the SFO and OVLT to downstream regions that control fluid intake and autonomic function; however, pathway-specific and stimulus-dependent mechanisms are not fully understood. These studies investigate how the MnPO differentially responds to models of physiological challenges that induce thirst, as well as pathway-specific mechanisms of blood pressure in a known model of hypertension. To study the role of the MnPO in thirst, rats were tested with models of cellular (hyperosmolality) and extracellular (angiotensin II, ANG II) dehydration associated with hypovolemia. Previous studies have shown that different populations of MnPO neurons are osmo- or ANG II-sensitive; however, both stimuli lead to a converging behavioral outcome: water consumption. This led to the hypothesis that osmotic challenges and ANG II activate MnPO neurons that project to different regions in a stimulus-dependent manner. Results show that the MnPO signals to specific thirst-driving regions of the brain and the activation of these regions is dependent on the stimulus. To study the role of the MnPO in regulating blood pressure, an experimental model of chronic intermittent hypoxia (CIH) associated with obstructive sleep apnea (OSA) is used to successfully mimic the oxygen deprivation associated with apneic breathing patterns patients with mild to moderate forms of OSA experience. Both patients with OSA and rodents in the CIH model develop diurnal hypertension, which is a sustained increase in blood pressure that persists into the waking hours. Hypertension involves multiple organ systems, including the central nervous system, and can be a heterogenous disease state that manifests from a number of factors, including CIH, ANG II from renin-angiotensin system (RAS), and changes in body fluid osmolality. This led to the hypothesis that pathway-specific inhibition of MnPO neurons that project to pre-autonomic neurons in the paraventricular nucleus (PVN) of the hypothalamus would block persistent hypertension. Results indicate that lesioning PVN-projecting MnPO neurons can block CIH-induced hypertension, resulting in decreases in oxidative stress and improved cardiovascular health. These findings provide new information about how the MnPO differentially regulates behavioral and physiological outcomes in a stimulus-dependent manner. These outcomes also have broad clinical implications relating to the role of the central nervous system in disease states affecting body fluid balance and blood pressure regulation.