Chronically increased intra-abdominal pressure produces systemic hypertension in dogs

Bloomfield, Geoffrey L.; Sugerman, Harvey J.; Blocher, Charles R.; Gehr, Todd W.B.; Sica, Dominic A.

doi:10.1038/sj.ijo.0801234

Cited by 37 publications

(17 citation statements)

References 35 publications

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“…This may stimulate renal sodium retention and may contribute to hypertension. In support of this hypothesis, artificially and chronically increasing intra-abdominal pressure in dogs resulted in hypertension (148). Cardiopulmonary Factors.…”

Section: Other Potential Hemodynamic Factorsmentioning

confidence: 58%

Obesity and Obesity-Initiated Metabolic Syndrome

Wahba

Mak

2007

Clinical Journal of the American Society of Nephrology

461

343

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There is an epidemic of obesity and the metabolic syndrome in the United States and across the world. Both entities are associated with high mortality, mainly as a result of cardiovascular disease. The epidemic of obesity has been paralleled by an increase in the incidence of chronic kidney disease (CKD). Several recent epidemiologic studies have shown that obesity and the metabolic syndrome are independent predictors of CKD. In addition to diabetes and hypertension, several other mechanisms have been postulated to initiate and maintain kidney injury in patients with obesity and the metabolic syndrome. This article reviews the recent epidemiologic data linking obesity and the metabolic syndrome to CKD and summarizes the potential mechanisms of renal injury in this setting, with a focus on the role of inflammation, lipotoxicity, and hemodynamic factors. Potential preventive and therapeutic modalities based on the limited evidence available are discussed.Clin , and the increase occurred for both men and women and for all age groups (2). Since then, the trend for increased prevalence has continued, particularly for adolescents and men (1). Obesity is also on the rise in other industrialized countries (3-5). The metabolic syndrome, previously known as syndrome X and a major consequence of obesity, is also on the rise (6). According to the Third National Health and Nutrition Examination Survey (NHANES III), the prevalence of the metabolic syndrome in the United States is 23% in those who are 20 yr or older and Ͼ40% in those who are 60 yr or older (7). According to the Third Adult Treatment Panel of the National Cholesterol Education Program, the metabolic syndrome is defined as the presence of at least three of the following criteria, with or without diabetes: Central obesity (waist circumference in men Ͼ102 cm and in women Ͼ88 cm), hypertriglyceridemia (Ն150 mg/dl), low HDL cholesterol (men Ͻ40 mg/dl, women Ͻ50 mg/dl), elevated fasting glucose (Ͼ110 mg/dl), and hypertension (Ն130/85 mmHg) (8). A central feature of the metabolic syndrome is insulin resistance, which results in hyperglycemia and hyperinsulinemia, and eventually leads to the development of diabetes (9). Central obesity is the most important predisposing factor for insulin resistance (9). Chronic inflammation is another feature of the metabolic syndrome, which, together with insulin resistance, results in complex metabolic derangements that contribute to the pathogenesis of hypertension, lipoprotein abnormalities, atherosclerosis, coronary artery disease, and other organ dysfunction (10,11). Both obesity and the metabolic syndrome are associated with high mortality, mainly related to cardiovascular disease (12,13). Overweight, obesity, and the metabolic syndrome have recently emerged as strong independent risk factors for chronic kidney disease (CKD) and ESRD. This article reviews the epidemiology of CKD in relationship to obesity and the metabolic syndrome and the possible mechanisms of renal injury that is caused by obesity and obesity-initiated metab...

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Section: Other Potential Hemodynamic Factorsmentioning

confidence: 58%

Obesity and Obesity-Initiated Metabolic Syndrome

Wahba

Mak

2007

Clinical Journal of the American Society of Nephrology

461

343

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“…This was confi rmed in a porcine model where a cinch was placed around the right renal vein after left nephrectomy which was associated with a decreased GFR, increased aldosterone and renin, as well as proteinuria [ 43 ]. In another study, we found that chronically elevated IAP in a canine model led to the progressive development of systemic hypertension which resolved with restoration of a normal IAP [ 44 ]. Others have suggested that the increased ICP with central obesity and increased IAP is responsible for hypertension via the central nervous system [ 42 ].…”

Section: Discussionmentioning

confidence: 65%

2 Pathophysiology of Obesity Comorbidity: The Effects of Chronically Increased Intra-abdominal Pressure

Sugerman

2014

Minimally Invasive Bariatric Surgery

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“…[41][42][43][44] Furthermore, experimentally induced reductions in splanchnic vascular capacitance elevate blood pressure via an increase in TPR. 45,46 Net transfer of even a small quantity of blood from veins into the arterial system could elicit an increase in vascular resistance through myogenic arterial contraction caused by activation and/or upregulation of voltage-sensitive calcium channels. 47 …”

Section: Discussionmentioning

confidence: 99%

Chronic Activation of Endothelin B Receptors

Fink

Lau

et al. 2007

Hypertension

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Abstract-Endothelin (ET) exerts powerful pressor actions primarily through activation of the ET A receptor subtype. The ET B receptor (ET B R) subtype, on the other hand, is generally thought to initiate physiological actions that decrease arterial pressure. Such actions include clearing ET from the bloodstream, initiating endothelium-mediated vasodilation, and facilitating renal sodium and water excretion. The effect of long-term activation of the ET B R on arterial pressure, however, never has been directly tested. In this study we evaluated cardiovascular responses to chronic (5-day) activation of ET B R in male rats using continuous intravenous infusion of the selective agonist sarafotoxin 6c. Surprisingly, we found that sarafotoxin 6c caused a sustained increase in arterial pressure that rapidly reversed on termination of infusion. The hypertension was associated with increased renal excretion of sodium and water and decreased plasma volume. Alterations in daily sodium intake did not affect the magnitude of the hypertension. Hemodynamic studies revealed a decreased cardiac output and increased total peripheral resistance during sarafotoxin 6c infusion. Infusion of sarafotoxin 6c caused a small increase in plasma ET levels. Nevertheless, the hypertension was not affected by coadministration of a selective ET A receptor antagonist (atrasentan) but was completely prevented by treatment with a combined ET A receptor and ET B R antagonist (A186280). These experiments reveal for the first time that chronic activation of ET B R in rats causes sustained hypertension. (Hypertension. 2007;50:512-518.)Key Words: endothelin Ⅲ ET B receptor Ⅲ salt Ⅲ hemodynamics E ndothelins (ETs) have powerful effects on arterial blood pressure regulation and contribute to the genesis of human and experimental hypertension. 1 Most ET-mediated pressor actions result from stimulation of the ET A receptor (ET A R) found in vascular smooth muscle, kidney, heart, adrenal gland, and other tissues. 1 The influence of ET B receptor (ET B R) on arterial pressure (AP) regulation has been more controversial, but the bulk of evidence supports an antihypertensive function. Knockout of the ET B R gene causes salt-sensitive hypertension in rats 2 and mice, 3,4 as does chronic pharmacological blockade of ET B R in a variety of species. 5-8 One important antihypertensive mechanism associated with ET B R activation may be enhanced renal sodium and water excretion, because renal-collecting, duct-specific knockout of ET B R causes hypertension. 9 Other studies, however, do not support a critical role for renal ET B R in controlling AP. 2 ET B Rs on endothelial cells act as plasma ET clearance receptors, 10 and their absence or blockade produces increased plasma ET levels that can activate ET A R to cause hypertension. 6 In addition, ET B Rs located on endothelial cells promote vasodilation by releasing NO and prostanoids. Nevertheless, endothelial cell ET B Rs do not seem necessary for chronic AP regulation, because their selective deletion does not cause...

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Chronically increased intra-abdominal pressure produces systemic hypertension in dogs

Cited by 37 publications

References 35 publications

Obesity and Obesity-Initiated Metabolic Syndrome

Obesity and Obesity-Initiated Metabolic Syndrome

2 Pathophysiology of Obesity Comorbidity: The Effects of Chronically Increased Intra-abdominal Pressure

Chronic Activation of Endothelin B Receptors

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