Browsing by Subject "blood pressure"
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Item Assessment of Obesity as a Cardiovascular Disease Risk Factor in a Geriatric Rural Texas Community - A Six Month Follow-Up(1999-12-01) Coustasse, Alberto; Antonio Rene; Doug A. Mains; Gilbert RamirezCoustasse, Alberto, Assessment of Obesity as a Cardiovascular Disease Risk Factor in a Geriatric Rural Texas Community – A Six Month Follow-up. Master of Public Health Track, Public Health Administration, December 1999, 22 pp., 9 tables, 9 illustrations, bibliography, 7 titles. The health fair approach was used as a method to establish individual and population health status baselines and to provide a mechanism to follow-up with an elderly population in a rural Texas community. A controlled trial sample of forty-four seniors was initially screened in a primary care clinic in August 1998. Patients were reevaluated at six months and results demonstrated a 46% increase in BMI [Body Mass Index]; 62% remained obese; 62% maintained elevated cholesterol or increased cholesterol values to abnormal values; 61% maintained or increased their BP [blood pressure] to abnormal values. A significant finding was that a change of one unit in the BMI correlated with a change of 19.88 mmHg [millimeter mercury] of SBP [systolic blood pressure] and 18.59 mmHg of DBP [diastolic blood pressure]. The societal economic impact of mortality and morbidity (without the benefit of target interventions) for the initial forty-four seniors was projected at & 74,949. Keywords: Health fairs; obesity; cardiovascular; cost; case management.Item Effects of Compression of the Fourth Ventricle on Sleep Latency(2003-05-01) Holland, Bradly Shane; Michael Smith; Russel Gamber; Scott StrollHolland, Bradly Shane, Effects of Compression of the Fourth Ventricle on Sleep Latency. Master of Science (Clinical Education and Research), May 2003, pp, 2 tables, 3 figures, references. Hypothesis: Compression of the fourth ventricle decreases sleep latency independent of therapeutic touch. Methods: Subjects participated in CV-4 treatment, sham treatment, and control. Order was randomized. Electrocardiogram and electroencephalogram tracings, heart rate, and blood pressure were recorded. After the treatments, data were collected for 30 minutes. Data were collected during the control for 30 minutes. After the first two treatments, subjects had a one hour recovery period. Results: The ANOVA showed a difference between groups (F=28.462, power=.998, p [less than] .001). Pairwise comparison showed sleep latency was shorter for CV-4 than sham or control. There was no difference between sham and control. For total percent sleep, an ANOVA showed a difference between groups (F=20.5, power=.982, p=.001). Pairwise comparison revealed differences between control and CV-4, control and sham, but not CV-4 and sham. Conclusions: CV-4 shortens sleep latency independent of light touch.Item Mechanisms of Chemoreflex Control of Muscle Sympathetic Nerve Activity and Blood Pressure in Humans(2004-05-01) Hardisty, Janelle M.; Smith, Michael; Shi, Xiangrong; Clark, MichaelHardisty, Janelle M., Mechanisms of Chemoreflex Control of Muscle Sympathetic Nerve Activity and Blood Pressure in Humans. Doctor of Philosophy (Integrative Physiology), May 2004. The mechanisms linking obstructive sleep apnea (OSA) and cardiovascular disease are not fully understood; however, studies report patients with OSA exhibit chronic elevations in muscle sympathetic nerve activity (MSNA). This appears to be due to altered chemoreflex control of MSNA, mediated primarily by hypoxia. Yet, a correlation between degree of hypoxia and chemoreflex control of MSNA is unknown. Therefore, it was evaluated whether degree of hypoxia occurring during apnea determines the sympathoexcitatory and blood pressure responses, and whether these responses are augmented in OSA patients. Additionally, it was studied whether altered chemoreflex function in OSA patients is predictive of blood pressure response to apnea. In a clinical setting, the blood pressure response to voluntary apnea was determined to evaluate whether this could be used as a non-invasive measure of chemoreflex gain in OSA. Finally, the effect of hyperoxia on MSNA was studied to determine whether 15 min of hyperoxia, following intermittent hypoxic apnea, reverses the elevation of MSNA and altered chemoreflex control of MSNA. Consistent with the hypotheses, a relationship between MSNA responses, blood pressure response and level of hypoxia were determined. MSNA and peak systolic pressure responses were augmented in OSA subjects (p≤0.05 and p≤0.05, respectively), as well as, chemoreflex gain (p≤0.05). Clinically, peak systolic pressure responses to apnea were augmented in OSA patients (p˂0.001). Finally, basal MSNA and chemoreflex control of MSNA, following hyperoxia, was not different from baseline through 180 min of recovery (p=0.940 and p=0.278, respectively). These data support the hypotheses that chemoreflex gain is predicative of the blood pressure response; and furthermore, the MSNA and blood pressure responses to hypoxic apnea are augmented in OSA. Additionally, peak systolic pressure responses to voluntary apnea are augmented in OSA. Additionally, peak systolic pressure responses to voluntary apnea are augmented in OSA patients and could possibly be used as a marker of chemoreflex gain. Moreover, these data support the hypothesis that hyperoxia can reverse basal sympathoexcitation and augmented chemoreflex control of MSNA, associated with hypoxic apnea, supporting that elevations in MSNA are hypoxia mediated.Item Met-Enkephalin-Arg-Phe (MERF) and Metabolism of MERF Across the Canine Heart Vascular Bed(2000-08-01) Pearlman, Eric Brian; Barbara Barron; Patricia A. Gwirtz; Michael L. SmithPearlman, Eric B., Met-Enkephalin-Arg-Phe (MERF) and Metabolism of MERF Across the Canine Heart Vascular Bed. Master of Science (Biomedical Science), August, 2000, 37 pp., 3 tables, 11 figures, references, 20 titles. Methionine enkephalin arginine phenylalanine (MERF) has been shown to be co-stored with catecholamines in vesicles. The catecholamines appear to decrease the degradation rate of 3H-MERF in vitro. The aim of this study is to investigate the spillover and metabolism of MERF across the canine heart vascular bed. I hypothesize that 3H-MERF is either degraded in the plasma or taken up and degraded by the heart. I further hypothesize that the exogenous catecholamine, isoproterenol, inhibits or reduces the rate of MERF degradation. Mongrel dogs were anesthetized and instrumented to record cardiovascular parameters, infuse 3H-MERF, and obtain blood samples across the heart. Blood samples were taken before and after stopping 3H-MERF infusion to evaluate kinetics, show steady state, and test the effect of treatments. Steady state concentration of 3H-MERF was observed after 30 min of infusion. Chromatography separated intact from degraded 3H-MERF. Three experimental groups were used: control, propranolol plus isoproterenol, and propranolol only. Blockade of β-receptors was necessary to prevent changes in coronary blood flow. Propranolol bolus (0.2 mg/kg) was administered IV at 50 min. 3 μg/min isoproterenol or 0.5 ml/min normal saline was infused starting at 70 min until the end of sample collection. The 3H-MERF venous-arterial (V-A) difference prior to treatment was negative, indicating degradation in the plasma or uptake and degradation by the heart. The 75 min V-A difference was used to calculate the effect of the infusions on the degradation or uptake of the 3H-MERF; this value was unchanged by any treatment. Spillover of 3H-MERF was significantly lower in the propranolol + isoproterenol dogs (p [less than] 0.05) compared to propranolol only treatment at 75 min. Heart rate was significantly lower for the propranolol only group compared to control. Blood pressure and change in coronary flow were unchanged. In conclusion, isoproterenol does not affect the metabolism of 3H-MERF across the canine heart vascular bed. Propranolol, however, does increase the intact 3H-MERF in the plasma, but additional β adrenergic blockade agents need to be investigated to determine the mechanism by which this takes place.Item Should Renal Inflammation Be Targeted While Treating Hypertension?(Frontiers Media S.A., 2022-06-13) Chaudhari, Sarika; Pham, Grace S.; Brooks, Calvin D.; Dinh, Viet Q.; Young-Stubbs, Cassandra M.; Shimoura, Caroline G.; Mathis, Keisa W.Despite extensive research and a plethora of therapeutic options, hypertension continues to be a global burden. Understanding of the pathological roles of known and underexplored cellular and molecular pathways in the development and maintenance of hypertension is critical to advance the field. Immune system overactivation and inflammation in the kidneys are proposed alternative mechanisms of hypertension, and resistant hypertension. Consideration of the pathophysiology of hypertension in chronic inflammatory conditions such as autoimmune diseases, in which patients present with autoimmune-mediated kidney inflammation as well as hypertension, may reveal possible contributors and novel therapeutic targets. In this review, we 1) summarize current therapies used to control blood pressure and their known effects on inflammation; 2) provide evidence on the need to target renal inflammation, specifically, and especially when first-line and combinatory treatment efforts fail; and 3) discuss the efficacy of therapies used to treat autoimmune diseases with a hypertension/renal component. We aim to elucidate the potential of targeting renal inflammation in certain subsets of patients resistant to current therapies.Item Single Nucleotide Polymorphisms and Haplotype Analyses of Complex Medical Disorders(2008-05-01) Gonzalez, Suzanne D.; Arthur Eisenberg; Robert Luedtke; Rustin ReevesGonzalez, Suzanne D., Doctor of Philosophy. Cell Biology and Genetics. Single Nucleotide Polymorphisms and Haplotype Analyses of Complex Medical Disorders. Number of Pages: 129. Number of Tables: 25. Number of Illustrations: 5. Number of Titles Included in References: 197. There has been great difficulty in identifying genes involved in complex disorders. The complex genetic basis of these diseases indicates that either several genes act together to cause disease, or genetic heterogeneity is present in the population. This dissertation was aimed at developing new assays to identify polymorphisms in novel candidate genes that potentially contribute to two classes of common complex disorders: psychiatric diseases and metabolic disorders. Genotyping assays were developed to investigate single nucleotide polymorphisms (SNPs) and haplotypes in complex genetic disorders using multiplexed SNP panels, restriction fragment length polymorphism technology, and cycle sequencing platforms. An introduction to the study is provided in Chapter 1. Manuscripts focus on association studies of candidate genes in Bipolar Disorder and Schizophrenia (Chapter 2), Type 2 Diabetes, Hypertension and Metabolic Syndrome (Chapter 3), and baseline blood pressure in African Americans (Chapter 4). The summary of these manuscripts (Chapter 5) describes the significant associations made between SNPs/haplotypes in psychiatric and metabolic complex genetic disorders. Significant genetic associations of SNPs within the PHLPP gene were detected among schizophrenics (Chapter 2). The G allele of SNP rs8087170 was associated with the control population with the T allele of SNP rs12966002 was found only in schizophrenics. A significant variance was detected at SNP rs12457020 between bipolar and schizophrenic datasets, as there was a 10 fold increase in the A allele in the bipolar group. Significant associations of ATP1A2 5’ SNPs C-1489T and G-1253A were detected in metabolic syndrome and hypertensive groups (Chapter 3). Haplotypes based on these 3 SNPs were significantly associated with metabolic syndrome and hypertensive populations. Four linked ATP1A2 SNPs, G3756C, G3853A, C3913T and C3915T, were associated with baseline blood pressure (Chapter 4). Haplotypes associated with blood pressure in an ethnic specific manner. GGCC associated with lower blood pressures, while haplotype GGTT associated with higher blood pressures in African Americans. These studies provide new mechanisms to identify mutations and provide evidence supporting the pathophysiology of these disorders.Item Single Nucleotide Polymorphisms of the ATP1a2 gene and Their Effects on Blood Pressure and Other Cardiovascular Variable in African Americans and Caucasian Americans(2007-05-01) Thakre, Tushar P.; Smith, Michael L.; Caffrey, James L.; Shi, XiangrongThakre, Tushar P., Single Nucleotide Polymorphisms of the ATP1a2 Gene and Their Effects on Blood Pressure and Other Cardiovascular Variables in African Americans and Caucasian Americans. Doctor of Philosophy (Integrative Physiology), May 2007. Mutations in the 3’ – untranslated region (3’-UTR) of the ATP1a2 gene, which encodes the α2 subunit of Na+-K+-ATPases are reportedly associated with hypertension. This study was initiated: 1) to identify and to determine the frequency of the single nucleotide polymorphism (SNP) responsible for a 3’-UTR restriction fragment length polymorphism (RFLP) of the ATP1a2 gene in African Americans (AAs) and Caucasian Americans (CAs), 2) to test for association of these SNPs with baseline blood pressure, 3) to determine whether pressor responses of cardiovascular variables are affected by these SNPs, and 4) to test whether endothelial dysfunction is associated with these SNPs. RFLP analysis using the BglII restriction enzyme was performed on DNA obstained from 63 normotensive subjects and results were confirmed by sequencing. Responses of blood pressure, heart rate, muscle sympathetic nerve activity (MSNA) and systematic vascular resistance (SVR) to pressor stimuli of two difference origins (cold pressor and hypoxic apnea) were tested in 37 individuals. Endothelin function was tested using ultrasound imaging of the brachial artery. Six SNPs were detected in the sequenced region at mRNA positions G3756C, A3788G, T3849C, G3853A, C3913T and C3915T, of which T3849C, G3853A and C3913T are novel SNPs. Mutant allel frequencies for these SNPs were higher in AAs than in CAs. SNPs at mRNA positions G3756C, G3853A, C3919T and C3915T were associated with baseline blood pressure. The ancestral haplotype G3756G3853AC3913C3915 constructed from these 4 SNPs associated with lower blood pressure in AAs and with higher blood pressure in CAs. Haplotypes GGTT and CATT were associated with higher mean and diastolic blood pressures, respectively in AAs. Responses of blood pressure, MSNA and SVR to the pressor stimuli were not difference across haplotype (p≥0.61). Similarly, no endothelial dysfunction was associated with the SNPs (p≥0.56). Haplotype groups associated with higher baseline blood pressure tended to have higher systemic vascular resistance (SVR), suggesting increased vascular tonicity as a primary mechanism for the higher blood pressure. These data suggest that although SNPs in the 3’-UTF of the ATP1a2 gene and haplotypes constructed from the SNPs affect baseline blood pressure in an ethnic-specific manner at a young age, neither the responses to pressor stimuli nor endothelial function are affected. Thus, these SNPs and haplotypes are associated with an increased arterial pressure that is likely mediated by an increased vascular tone.Item Sympathetic Responses to Dynamic Arm Ergometry in Humans(2001-05-11) Wasmund, Stephen Lee; Patricia A. Gwirtz; Peter B. Raven; H. Fred DowneyWasmund, Stephen L, Sympathetic Responses to Dynamic Arm Ergometry. Doctor of Philosophy (Biomedical Sciences), May 2001; 96 pp; 1 table; 15 figures; bibliography. Cardiovascular control during exercise is of obvious importance due to the need for an increase in cardiac output and maintenance of blood pressure when metabolic demands increase. While investigations during exercise have been conducted for some time, and much is known about the responses to dynamic exercise, the understanding of the signals that elicit the cardiovascular changes, particularly as mediated by sympathetic nerve activity (SNA) is incomplete. Sympathetic nerve activity plays an important role during exercise by causing vasoconstriction in non-working vascular beds, probably causing vasoconstriction in the vascular beds of working muscles to partially counteract the profound vasodilation caused by locally produced metabolites and by stimulating the heart to increase contractility and heart rate. It is possible to directly measure electrical activity in sympathetic nerves supplying the vasculature of skeletal muscles, however few investigations have reported on this activity during strenuous dynamic exercise. The investigations described in this dissertation extend the understanding of muscle sympathetic nerve responses to dynamic exercise. The first investigation evaluated SNA during a graded arm ergometry test to near volitional fatigue and demonstrated that increases in SNA began to occur at approximately 40% of peak exercise and then increase in a linear fashion until exercise is stopped. This relation is more closely linked to relative workload rather than heart rate as previously suggested. We also sought to determine the relationship between the increase in SNA and the ventilator threshold, hypothesizing that the two would occur at similar times, and concluded that the exercise protocol utilized did not elicit a distinct breakpoint in ventilation. However, a ventilator threshold did occur in two subjects and there appeared to be an accelerated increase in SNA. The second investigation assessed the dynamics of SNA, blood pressure and heart rate responses during the onset and termination of dynamic arm ergometry at mild, moderate and intense workloads to determine the relationship between changes in sympathetic nerve activity and blood pressure. When analyzing data every 10 seconds we determined that modest increases in SNA tend to occur at the onset of exercise in most subjects, but this response did not reach significance. This finding suggests that a neural mechanism, likely central command, plays a minor role in the initial activation of SNA, although this is probably attenuated or overridden by cardiopulmonary reflex mediated sympathoinhibition as has been previously proposed. The delay (30 s) in frank sympathetic nerve activation during strenuous exercise strongly suggests that a delayed signal, probably muscle metaboreceptor stimulation, is the primary stimulus for activation of SNA. At the termination of 5 minutes of exercise SNA, blood pressure and heart rate all decreased significantly below peak values within 10 seconds. We propose that metabolites rapidly drop below a threshold level that allows SNA to decrease significantly towards baseline values. A rapid control mechanism, such as central command or mechanoreceptor stimulation, might also play an important role in returning SNA towards resting values following exercise. We conclude that SNA remains active throughout relatively strenuous dynamic exercise, and that multiple control mechanisms are likely responsible for its control during the onset and termination of exercise.Item The Role of Angiotensin II in Central Control of Blood Pressure and Body Fluid Homeostasis(2016-08-01) Shell, Brent; Cunningham, J. Thomas; Mifflin, Steve W.; Schreihofer, Ann M.The brain Renin Angiotensin System (RAS) is quickly becoming recognized as a critical mediator of blood pressure and body fluid homeostasis. In the forebrain, the median preoptic nucleus (MnPO) responds to Angiotensin II (Ang II) stimulation by increasing thirst and blood pressure. Understanding how this nuclei regulates blood pressure and body fluid homeostasis in response to Ang II has the potential to open new therapeutic avenues for treatment of hypertension. In the studies following series of studies I investigated the role of MnPO Angiotensin Type Ia receptors in the sustained hypertension induced by Chronic Intermittent Hypoxia (CIH) and thirst regulation. The first project focuses on the role of the MnPO in the sustained hypertension of CIH. Sleep apnea leads to hypertension that persists throughout the waking period. The neural mechanisms that underlie this pathophysiological increase in blood pressure are not well known. CIH is a model of the hypoxemia experienced by sleep apnea sufferers. This model produces a sustained increase in blood pressure, and numerous studies have indicated that the central renin-angiotensin system is involved in this prolonged hypertension. The MnPO receives inputs from the subfornical organ (SFO) and the organum vasculosum lamina terminalis, both circumventricular organs (CVOs) outside the blood brain barrier allowing for it to receive input from nuclei exposed to peripherally circulating hormones. Downstream the MnPO projects to brain regions that control sympathetic activity, such as the paraventricular nucleus (PVN), making it a prime target for integrating peripheral signals with central sympathetic drive. Previous studies have shown that administration of Losartan, and AT1 receptor blocker, directly into the ventricles of the brain prevents the sustained component of CIH induced hypertension and decreaeses FosB in the MnPO. Inhibition of the transcription factor FosB in the median preoptic nucleus via a dominant negative construct prevents the sustained hypertension from CIH. CIH also increases Angiotensin Type 1a receptor mRNA in the MnPO via the FosB transcription factor. We hypothesize that knockdown of AT1a receptors locally in the MnPO will prevent the sustained hypertension of CIH. Utilizing a short hairpin RNA we knocked down the Angiotensin Type 1a receptor in the MnPO to determine its contribution to 7 days of CIH hypertension. AT1a receptor knockdown in the median preoptic nucleus blocked the sustained component of hypertension from CIH as compared to scramble injected animals. Immunohistochemistry revealed significantly less FosB positive cells in the MnPO of animals injected with the knockdown vector compared to animals given the control vector prior to 7 days of CIH. The rostral ventrolateral medulla, a key regulator of sympathetic outflow, also expressed significantly less FosB with the AT1a knockdown in the MnPO. Our results indicate that AT1a receptors in the MnPO are regulated by FosB and contribute to CIH hypertension. Thirst is a critical function the MnPO regulates and the second project aimed to determine if Ang II is necessary for thirst generation at the MnPO. Ang II is known to produce a dipsogenic response when administered peripherally, or centrally. Peripheral Ang II acting as a hormone activates CVOs, brain regions lacking a blood brain barrier, such as the SFO. These circumventricular organs synapse upon the MnPO which leads to activation of higher cortical centers and thirst. Intracerebroventricular (ICV) administration of Ang II produces thirst without interacting with CVOs by directly activating the MnPO, and it is therefore hypothesized that Ang II is the neurotransmitter released at the CVO-MnPO junction. We sought to test this hypothesis by knocking down AT1a receptors in the MnPO using a short hairpin RNA complimentary for the receptor subtype. Knockdown of AT1a in the MnPO significantly reduced drinking in animals administered ICV Ang II. This reduction in water consumption was mirrored by a reduction in cFos, a transcription factor and marker of neuronal activity, in the MnPO, SON, and PVN. Thirst generated by subcutaneous administration of Ang II was unaffected by the knockdown of AT1a in the MnPO. cFos counts in the SFO, OVLT, MnPO, PVN, and SON also were not significantly influenced. These data indicates that AT1a receptors in the MnPO are not necessary for water intake stimulated by peripheral Ang II. While experimental administration of Ang II directly to the ventricles is sufficient to induce drinking it may not play a prominent role in stimulating drinking under physiological conditions.