Morbid Obesity, Hypertensive Disease and the Renin-Angiotensin-Aldosterone Axis

Ruano, M; Silvestre, V.; Castro, R. B.; García-Lescún, M. C. G.; Rodríguez, Ana; Marco, Ángel; García-Blanch, G

doi:10.1381/0960892053923734

Cited by 71 publications

(53 citation statements)

References 20 publications

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“…Various studies have demonstrated increased plasma renin activity and plasma angiotensinogen, angiotensin II and aldosterone levels in obese individuals. [16][17][18] Cooper et al pointed out that the ACE insertion/ deletion polymorphism was linked to changes in ACE levels, but was inconsistently associated with BMI. A study of a Saudi population noted a higher frequency of the mutant deletion allele in hypertensive cases with a BMI of ≥30 kg/m 2 in comparison to controls, although the difference was not significant.…”

Section: Discussionmentioning

confidence: 99%

Association of Angiotensin-Converting Enzyme and Glutathione S-Transferase Gene Polymorphisms with Body Mass Index among Hypertensive North Indians

Rizvi

Raza

Siddiqi

et al. 2015

SQUMJ

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abstract:Objectives: This study aimed to examine the association of angiotensin-converting enzyme (ACE) and glutathione S-transferase (GST) gene polymorphisms with body mass index (BMI) in hypertensive North Indians. Methods: This case-control study was carried out between May 2013 and November 2014 at the Era's Lucknow Medical College & Hospital, Lucknow, India, and included 378 subjects divided into three groups. One group constituted 253 hypertensive individuals (sustained diastolic blood pressure of >90 mmHg and systolic blood pressure of >140 mmHg) who were subcategorised according to normal (<25 kg/m 2 ) or high (≥25 kg/m 2 ) BMI. The third group consisted of 125 age-, gender-and ethnically-matched normotensive controls with a normal BMI. Gene polymorphisms were evaluated by polymerase chain reaction. The genotypic and allelic frequency distribution among both groups were analysed. Results: A significant difference was found between GST theta 1-null and GST mu 1-positive genotype frequencies among the hypertensive overweight/obese individuals and controls (P = 0.014 and 0.033, respectively). However, no difference was observed in the frequency of ACE polymorphisms. ACE insertion/insertion genotype (P = 0.006), insertion and deletion alleles (P = 0.007 each) and GST theta 1-null and GST theta 1-positive genotypes (P = 0.006 each) were found to differ significantly between hypertensive cases and controls, regardless of BMI. Conclusion: ACE and GST gene polymorphisms were not associated with BMI but were significantly associated with hypertension among the studied group of North Indians.

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Section: Discussionmentioning

confidence: 99%

Association of Angiotensin-Converting Enzyme and Glutathione S-Transferase Gene Polymorphisms with Body Mass Index among Hypertensive North Indians

Rizvi

Raza

Siddiqi

et al. 2015

SQUMJ

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“…19 Improvements in both neuroendocrine and cytokine profiles have been described following BAS. 20,21 Patients with MO have abnormal circulating levels of a variety of adipocyteassociated cytokines, including leptin, 22 and normalization of cytokine profiles has been described following surgery. 21 …”

Section: Discussionmentioning

confidence: 99%

Safety and Efficacy of Bariatric Surgery in Morbidly Obese Patients with Severe Systolic Heart Failure

Ramani

McCloskey

Ramanathan

et al. 2008

Clinical Cardiology

104

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Background: Morbid obesity (MO) is a risk factor for congestive heart failure (CHF). The presence of MO impairs functional status and disqualifies patients for cardiac transplantation. Bariatric surgery (BAS) is a frontline, durable treatment for MO; however, the safety and efficacy of BAS in advanced CHF is unknown. Hypothesis: We hypothesized that by utilizing a coordinated approach between an experienced surgical team and heart failure specialists, BAS is safe in patients with advanced systolic CHF and results in favorable outcomes. Methods: We performed a retrospective chart review of 12 patients with MO (body mass index [BMI] 53±7 kg/m 2 ) and systolic CHF (left ventricular ejection fraction [LVEF] 22±7%, New York Heart Association [NYHA] class 2.9±0.7) who underwent BAS, and then compared outcomes with 10 matched controls (BMI 47.2±3.6 kg/m 2 , LVEF 24±7%, and NYHA class 2.4±0.7) who were given diet and exercise counseling. Results: At 1 y, hospital readmission in BAS patients was significantly lower than controls (0.4±0.8 versus 2.5±2.6, p = 0.04); LVEF improved significantly in BAS patients (35±15%, p = 0.005), but not in controls (29±14%, p = not significant [NS]). The NYHA class improved in BAS patients (2.3±0.5, p = 0.02), but deteriorated in controls (3.3±0.9, p = 0.02). One BAS patient was successfully transplanted, and another listed for transplantation. Conclusions: Bariatric surgery is safe and effective in patients with MO and severe systolic CHF, and should be considered in patients who have failed conventional therapy to improve clinical status.

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“…[23][24][25] Hall et al 19 reported a more than twofold increase in plasma renin activity after a 5-week period of highfat diet administration in conscious dogs. Moreover, fat restriction succeeded in diminishing the values of the RAS components, indicating the possibility that the degree of adiposity might have a direct influence in this BP-regulating system.…”

Section: Function Of Ras In Obesity Hypertensionmentioning

confidence: 99%

Mechanisms of obesity-induced hypertension

et al. 2010

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The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

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Morbid Obesity, Hypertensive Disease and the Renin-Angiotensin-Aldosterone Axis

Cited by 71 publications

References 20 publications

Association of Angiotensin-Converting Enzyme and Glutathione S-Transferase Gene Polymorphisms with Body Mass Index among Hypertensive North Indians

Association of Angiotensin-Converting Enzyme and Glutathione S-Transferase Gene Polymorphisms with Body Mass Index among Hypertensive North Indians

Safety and Efficacy of Bariatric Surgery in Morbidly Obese Patients with Severe Systolic Heart Failure

Mechanisms of obesity-induced hypertension

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