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Excess weight gain, especially when associated with increased visceral adiposity, is a major cause of hypertension, accounting for 65–75% of the risk for human primary (essential) hypertension. Increased renal tubular sodium reabsorption impairs pressure natriuresis and plays an important role in initiating obesity hypertension. The mediators of abnormal kidney function and increased blood pressure during development of obesity hypertension include 1) physical compression of the kidneys by fat in and around the kidneys, 2) activation of the renin-angiotensin-aldosterone system (RAAS), and 3) increased sympathetic nervous system (SNS) activity. Activation of the RAAS system is likely due, in part, to renal compression as well as SNS activation. However, obesity also causes mineralocorticoid receptor activation independent of aldosterone or angiotensin II. The mechanisms for SNS activation in obesity have not been fully elucidated but appear to require leptin and activation of the brain melanocortin system. With prolonged obesity and development of target organ injury, especially renal injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes, and inflammation. Unless effective anti-obesity drugs are developed, the impact of obesity on hypertension and related cardiovascular, renal and metabolic disorders is likely to become even more important in the future as the prevalence of obesity continues to increase.

Obesity is a major risk factor for essential hypertension, diabetes, and other comorbid conditions that contribute to development of chronic kidney disease. Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion via activation of the sympathetic nervous system and renin–angiotensin–aldosterone system and by physical compression of the kidneys, especially when there is increased visceral adiposity. Other factors such as inflammation, oxidative stress, and lipotoxicity may also contribute to obesity-mediated hypertension and renal dysfunction. Initially, obesity causes renal vasodilation and glomerular hyperfiltration, which act as compensatory mechanisms to maintain sodium balance despite increased tubular reabsorption. However, these compensations, along with increased arterial pressure and metabolic abnormalities, may ultimately lead to glomerular injury and initiate a slowly developing vicious cycle that exacerbates hypertension and worsens renal injury. Body weight reduction, via caloric restriction and increased physical activity, is an important first step for management of obesity, hypertension, and chronic kidney disease. However, this strategy may not be effective in producing long-term weight loss or in preventing cardiorenal and metabolic consequences in many obese patients. The majority of obese patients require medical therapy for obesity-associated hypertension, metabolic disorders, and renal disease, and morbidly obese patients may require surgical interventions to produce sustained weight loss.

Excessive adiposity raises blood pressure and accounts for 65-75% of primary hypertension, which is a major driver of cardiovascular and kidney diseases. In obesity, abnormal kidney function and associated increases in tubular sodium reabsorption initiate hypertension, which is often mild before the development of target organ injury. Factors that contribute to increased sodium reabsorption in obesity include kidney compression by visceral, perirenal and renal sinus fat; increased renal sympathetic nerve activity (RSNA); increased levels of anti-natriuretic hormones, such as angiotensin II and aldosterone; and adipokines, particularly leptin. The renal and neurohormonal pathways of obesity and hypertension are intertwined. For example, leptin increases RSNA by stimulating the central nervous system proopiomelanocortin-melanocortin 4 receptor pathway, and kidney compression and RSNA contribute to renin-angiotensin-aldosterone system activation. Glucocorticoids and/or oxidative stress may also contribute to mineralocorticoid receptor activation in obesity. Prolonged obesity and progressive renal injury often lead to the development of treatment-resistant hypertension. Patient management therefore often requires multiple antihypertensive drugs and concurrent treatment of dyslipidaemia, insulin resistance, diabetes and inflammation. If more effective strategies for the prevention and control of obesity are not developed, cardiorenal, metabolic and other obesity-associated diseases could overwhelm health-care systems in the future. Obesity and its adverse consequences are major burdens to health-care systems worldwide 1. The Global Burden of Disease study, which includes data from 195 countries, reports that

This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. Mean arterial pressure, cardiac output, and heart rate were monitored 24 hours a day using computerized methods, water and electrolyte balances were measured daily, and renal hemodynamics were measured each week during the control period and 5 weeks of a high-fat diet. After 7 to 10 days of control measurements, 0.5 to 0.9 kg of cooked beef fat was added to the regular diet, and sodium intake was maintained constant at 76 mmol/d throughout the study. After 5 weeks of the high-fat diet, body weight increased from 24.0±1.0 to 35.9±4.9 kg, mean arterial pressure increased from 83±5 to 100±4 mm Hg, cardiac output increased from 2.86 ±0.27 to 4.45 ±0.55 L/min, and heart rate rose from 68 ±5 to 107 ±9 beats per minute. Associated with the hypertension was an increase in cumulative sodium balance to 507 ±107 mmol after 35 days and a rise in sodium iothalamate space, an index of extracellular fluid volume, to 131 ±4% of control. Sodium retention was due to increased tubular reabsorption, because glomerular filtration rate and effective renal plasma flow increased throughout the 5 weeks of the high-fat diet, averaging 135 ±4% and 149±19% of control, respectively, during the fifth week of the high-fat diet. Plasma renin activity and plasma insulin concentration increased from 0.46±0.12 ng angiotensin I/mL per hour and 11.1±2.6 (iXS/mL, respectively, to 1.10±0.23 ng angiotensin I/mL per hour and 30.1 ±7.0 fiU/mL after 5 weeks. Because decreased sodium excretion occurred despite elevated mean arterial pressure, obesity-induced hypertension in dogs is associated with a shift of renal pressure natriuresis that is caused by increased tubular reabsorption, although the exact mechanism by which this occurs is still unclear. W eight gain appears to be an important factor in elevating blood pressure in many essential hypertensive individuals. 14 Epidemiological studies have shown that hypertension is more prevalent in obese than in nonobese individuals and that blood pressure is correlated to body weight, even in normotensive subjects. "5 Experimental studies have demonstrated that weight gain, even over a period of a few weeks, consistently elevates blood pressure and weight loss decreases blood pressure independent of changes in sodium intake. "10 Although this association between obesity and hypertension is widely recognized, the mechanisms responsible for weight-related changes in blood pressure have not been elucidated.Much of the evidence for various mechanisms postulated to cause obesity-induced hypertension derives from studies that have attempted to correlate various abnormalities in obesity with hypertension. Establishing cause-and-effect relations has been hampered by the lack of suitable animal models that mimic obesityinduced hypertension in humans and that allow sequen-

Angiotensin II (ANG II) is one of the body's most powerful regulators of Na excretion, operating through extrarenal mechanisms, such as stimulation of aldosterone secretion, as well as intrarenal mechanisms. Considerable evidence suggests that the intrarenal actions of ANG II are quantitatively more important than changes in aldosterone secretion in the normal day-to-day regulation of Na balance and arterial pressure. ANG II at physiological concentrations increases proximal tubular reabsorption, but further studies are needed to determine whether ANG II also has an important effect on more distal tubular segments. ANG II also markedly constricts efferent arterioles, tending to increase Na reabsorption by altering peritubular capillary physical forces and also helping to prevent excessive decreases in glomerular filtration rate. ANG II may also decrease Na excretion and increase urine concentrating ability by reducing renal medullary blood flow. Regulation of Na excretion by ANG II is closely linked with arterial pressure control and volume homeostasis through the renal pressure natriuresis mechanism. Under many physiological conditions, such as changes in Na intake, ANG II greatly multiplies the effectiveness of the pressure natriuresis mechanism to prevent fluctuations in body fluid volume and arterial pressure. In circumstances associated with circulatory depression, such as decreased cardiac function, reductions in blood pressure and increased ANG II formation cause Na retention until arterial pressure is restored to normal. However, in pathophysiological conditions in which ANG II is inappropriately elevated, increased arterial pressure (hypertension) is required for the kidney to "escape" the potent antinatriuretic actions of ANG II and to return Na excretion to normal via the pressure natriuresis mechanism.

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PurposeBased on the theoretical framework of expectancy‐disconfirmation paradigm, the purpose of this paper is to examine the differences in student perceptions of the level of satisfaction related to educational and non‐educational services among four groups of international postgraduate business students from China, India, Indonesia and Thailand undertaking study in Australia.Design/methodology/approachThe data used in this study were derived from a mail survey conducted among international postgraduate business students from Asia studying at five universities in the state of Victoria, Australia. A total of 573 usable responses were received. Analysis using structural equation modelling, multivariate analysis of variance (MANOVA) and analysis of variance (ANOVA) was undertaken.FindingsThis study develops and tests a model of international postgraduate student satisfaction. Findings indicate that the importance of service quality factors related to both educational and non‐educational services varies among nationality groups and, therefore, has a differential impact on student satisfaction.Practical implicationsThe study provides insights into seven constructs related to educational and non‐educational services that are perceived as important by postgraduate business students from Asia in satisfaction formation. Universities should develop a diversified strategic marketing plan that incorporates the differential needs of international postgraduate business students according to the educational and non‐educational constructs developed in this paper.Originality/valueThis study makes a contribution by filling a void in academic research in the area of satisfaction in relation to postgraduate international business students from four nationality groups in Asia.