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Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndromeBrillante, Divina Graciela, Clinical School - St George Hospital, Faculty of Medicine, UNSW January 2008 (has links)
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
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Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndromeBrillante, Divina Graciela, Clinical School - St George Hospital, Faculty of Medicine, UNSW January 2008 (has links)
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
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Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndromeBrillante, Divina Graciela, Clinical School - St George Hospital, Faculty of Medicine, UNSW January 2008 (has links)
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
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Leptin : a risk marker for cardiovascular diseaseSöderberg, Stefan January 1999 (has links)
A major cause of morbidity and early death in the Western societies is cardiovascular disease (CVD) secondary to atherosclerotic disease. Metabolic aberrations have been linked to CVD. Particular combinations of these so-called risk markers are common and (central) obesity, Type 2 diabetes, impaired glucose tolerance, hypertension, dyslipidemia, dysfibrinolysis and hyperinsulinemia are often associated. This has been entitled the Insulin Resistance Syndrome (1RS), due to underlying insulin resistance. Moreover, aberrations in circulating levels of androgens and IGF-binding proteins are associated with 1RS. The main hypothesis in this thesis was that increased levels of leptin, the recently discovered adipocyte derived hormone in combination with obesity may be an important factor in the link between 1RS and the development of CVD. The association between leptin levels and variables associated with the Insulin Resistance Syndrome was studied in a healthy sample (n=163) of middle-aged men and women from the northern Sweden MONICA health survey. Central obesity was associated with high levels of leptin and insulin in men and women. In contrast, central obesity was linked to low testosterone levels in men, whereas in women, central obesity was associated with high testosterone but low SHBG levels. Furthermore, in males and postmenopausal women central obesity was a major determinant for circulating leptin. Leptin levels were associated with biochemical androgenicity in non-obese men and women. The direction of this association was dependent on gender and body fat distribution. Specifically, testosterone was inversely associated to leptin in non-obese men and in normal weight women whereas testosterone was positively associated to leptin in non-obese women. In contrast, adiposity and insulin levels, but not testosterone, were associated to leptin in obese men and women. Similarly, leptin was associated to IGFBP-1 and proinsulin in non-obese men and premenopausal women. Hyperleptinemia was significantly associated to high PAI-1 levels in men and in centrally obese women. In a multivariate model, high leptin levels predicted PAI-1 levels in men but not in women. Finally, leptin levels were related to blood pressure in obese men. The impact of hyperleptinemia on future risk for development of CVD was tested in a nested case-referent study based on the MONICA and the Västerbotten Intervention Program surveys. It was found that hyperleptinemia and high total cholesterol levels were associated with increased risk for development of myocardial infarction whereas high levels of apolipoprotein A-l were protective. Hyperleptinemia together with hypertension remained as significant risk markers for hemorrhagic stroke whereas hypertension alone predicted ischemic stroke. The combinations of hyperleptinemia on one hand and low apolipoprotein A- 1 and high blood pressure on the other were associated with a pronounced increased risk for myocardial infarction and hemorrhagic stroke, respectively. In conclusion, hyperleptinemia is independently associated with several risk markers for CVD included in the insulin resistance syndrome. Furthermore, high leptin levels predict the development of CVD. / <p>Härtill 5 uppsatser</p> / digitalisering@umu
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Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndromeBrillante, Divina Graciela, Clinical School - St George Hospital, Faculty of Medicine, UNSW January 2008 (has links)
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
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Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndromeBrillante, Divina Graciela, Clinical School - St George Hospital, Faculty of Medicine, UNSW January 2008 (has links)
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
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Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndromeBrillante, Divina Graciela, Clinical School - St George Hospital, Faculty of Medicine, UNSW January 2008 (has links)
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
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Muscle Morphology and the Insulin Resistance Syndrome : A Population-Based Study of 70 Year-Old-Men in UppsalaHedman, Anu January 2001 (has links)
<p>Skeletal muscle accounts for the largest part of insulin-mediated glucose uptake. Insulin resistance (IR) is the main component of insulin resistance syndrome (IRS) and is an essential cause of a number of cardiovascular risk factors. This thesis investigates the relationships between muscle morphological characteristics and IRS because skeletal muscle is responsible for the majority of glucose uptake.</p><p>In this population-based sample of 70-year-old men, higher proportion of type I fibers as well as higher capillarization were related to higher insulin sensitivity and higher self-reported physical activity, which were related to a lower prevalence of type IIB fibers. Serum triglycerides, HDL cholesterol and plasminogen activator inhibitor-1 (PAI-1) activity were significantly related to fiber distribution and muscle capillarization and muscle morphology, in part, explained the association between these metabolic risk factors with physical activity level. BMI, glucose intolerance, PAI-1 activity, serum FFA concentration, proportion of type IIB fibers, HDL cholesterol level, drug treatment, physical activity level, and W/H ratio together explained 55% of the variation in the insulin sensitivity index. In addition, almost a twofold improvement of the correlations was seen after correcting for intraindividual variation. Glucose tolerant hypertensive subjects showed a lower capillary supply when compared to controls. Capillary density was negatively correlated to the increase in mean arterial pressure over two decades as well as to supine heart rate 20 years before. Interestingly, supine heart rate showed an independent inverse association to the percentage of type I fibers and a positive correlation to the percentage of type IIB muscle fibers. Capillary density and elevated serum free fatty (FFA) acid values were inversely associated with insulin-mediated blood flow and thus to endothelial dysfunction, which has been linked to IR. In fact, capillary density and serum FFA level together explained 71% of the variation in insulin-mediated leg blood flow changes.</p><p>In conclusion, these population-based findings support the observations that muscle morphological features and insulin sensitivity are related to each other. Muscle morphology might explain some of the beneficial impact of physical activity on the components of IRS. Accordingly, we suggest that alterations in muscle morphology should be considered as an essential part of the IRS.</p>
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Muscle Morphology and the Insulin Resistance Syndrome : A Population-Based Study of 70 Year-Old-Men in UppsalaHedman, Anu January 2001 (has links)
Skeletal muscle accounts for the largest part of insulin-mediated glucose uptake. Insulin resistance (IR) is the main component of insulin resistance syndrome (IRS) and is an essential cause of a number of cardiovascular risk factors. This thesis investigates the relationships between muscle morphological characteristics and IRS because skeletal muscle is responsible for the majority of glucose uptake. In this population-based sample of 70-year-old men, higher proportion of type I fibers as well as higher capillarization were related to higher insulin sensitivity and higher self-reported physical activity, which were related to a lower prevalence of type IIB fibers. Serum triglycerides, HDL cholesterol and plasminogen activator inhibitor-1 (PAI-1) activity were significantly related to fiber distribution and muscle capillarization and muscle morphology, in part, explained the association between these metabolic risk factors with physical activity level. BMI, glucose intolerance, PAI-1 activity, serum FFA concentration, proportion of type IIB fibers, HDL cholesterol level, drug treatment, physical activity level, and W/H ratio together explained 55% of the variation in the insulin sensitivity index. In addition, almost a twofold improvement of the correlations was seen after correcting for intraindividual variation. Glucose tolerant hypertensive subjects showed a lower capillary supply when compared to controls. Capillary density was negatively correlated to the increase in mean arterial pressure over two decades as well as to supine heart rate 20 years before. Interestingly, supine heart rate showed an independent inverse association to the percentage of type I fibers and a positive correlation to the percentage of type IIB muscle fibers. Capillary density and elevated serum free fatty (FFA) acid values were inversely associated with insulin-mediated blood flow and thus to endothelial dysfunction, which has been linked to IR. In fact, capillary density and serum FFA level together explained 71% of the variation in insulin-mediated leg blood flow changes. In conclusion, these population-based findings support the observations that muscle morphological features and insulin sensitivity are related to each other. Muscle morphology might explain some of the beneficial impact of physical activity on the components of IRS. Accordingly, we suggest that alterations in muscle morphology should be considered as an essential part of the IRS.
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Die onderlinge verband tussen fisieke aktiwiteit, obesiteit en arteriële meegewendheid by 19-56-jarige vroue : POWIRS II-studie / Sulize NolteNolte, Sulize January 2004 (has links)
Several research studies indicate the increasing problem obesity has become
over the past few decades (Andersen 1999:41; Fox, 1999:56-60; Kuczmarshi et
al., 1994:205-212). Obesity, after cigarette smoke, is the leading cause of death
in the USA and a combination of diet factors and physical inactivity (two primary
contributors of obesity) leads to an average of 300,000 deaths per year
(McGinnis & Foege, 1993:2207-2212).
Previously little information was available on the effect of obesity on the
peripheral vascularization, and even less about the effect of obesity on arterial
compliance (Raison et al., 1998:299-303). Research indicated a decrease in
arterial compliance with an increase in body weight (Kumaran et al., 2002:7;
Sutton-Tyrrell et al., 2001:431; Tounian et al., 2001:1400-1404; Stepniakowski &
Egan, 1995:R567) however, contradictory research where no association
between obesity and arterial compliance was indicated, has also been found
(Singhal et al., 2002:1920; Mangoni et al., 1995:986). Mackey et al. (2002:16)
also found that an increased aortic stiffness is positively associated with lowered
physical activity levels.
A lifestyle consisting of moderate physical activity, has a positive effect on the
health, lowering of chronic illness risks, the prevention of cardiovascular diseases
and the improvement of quality of lie in overweight and obese patients (Adams
et al., 2003542; Ferreira et al., 2003:1670-1678; Macera, 2003:123; Mclnnis,
200396; Kolden et al., 2002:447). Moderate aerobic exercise is also seen as a
potential non-pharmaceutical therapeutic method to increase age associated
decrease in arterial compliance in young, middle aged and older adults (Gates et
al., 2003:2213; Havlik et al., 2003:156; Seals, 2003:68; Moreau et al., 2003:865;
Joyner, 2000:1214; Cameron et al., 1999:653).
The objective of this study was firstly to determine the correlation between
obesity and vascular function in Caucasian women between the ages 19 and 56
and to determine which marker of obesity is the best predictor of a weakened
vascular function (see article one). The second objective was to determine the
correlation between physical activity, obesity and arterial compliance in
Caucasian women between the ages 19 and 56 years (see article 2). A total of
115 Caucasian women were recruited to participate in this study. Anthropometric
measurements and a comprehensive body composition profile was taken using
the BOD POD. The Finometer apparatus was used to measure the arterial
compliance and the sphygmomanometer to measure the subjects blood
pressure. The subjects completed the Yale Physical Activity Survey questionnaire
to determine their physical activity index.
This study seems to indicate a positive relationship between arterial compliance
and obesity which could be explained by the influence blood volume had in
determining arterial compliance. A negative correlation was found between
obesity and blood pressure where an increase in obesity caused an increase in
both systolic and diastolic blood pressure. A positive correlation was found
between physical activity and obesity. The higher the activity levels were in this
study, the less obese the subjects tended to be. No correlation was found
between physical activity and arterial compliance. A clear trend, even though no
statistically significant differences, was found between physical activity and blood
pressure. The more active the subjects were, the lower their blood pressure
tended to be. / Thesis (M.Sc. (Human Movement Science))--North-West University, Potchefstroom Campus, 2005
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