Hypertension in Obesity

Kurukulasuriya, L. Romayne; Stas, Sameer; Lastra, Guido; Manrique, Camila; Sowers, James R.

doi:10.1016/j.ecl.2008.06.002

Cited by 42 publications

(37 citation statements)

References 86 publications

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“…Obesity is firmly established as a cause of hypertension, although additional mechanisms besides hyperinsulinemia have been proposed as mechanisms (35,42,56,63). Therefore, it is not surprising that a sodium-retaining action of insulin has continued to be advanced as a contributing factor for sodium retention and hypertension in obesity or metabolic syndrome (53,77,80).…”

Section: Conclusion 1: Insulin Is a Sodium Retainermentioning

confidence: 99%

Sodium-retaining effect of insulin in diabetes

Brands¹,

Manhiani²

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Brands MW, Manhiani MM. Sodium-retaining effect of insulin in diabetes. Am J Physiol Regul Integr Comp Physiol 303: R1101-R1109, 2012. First published October 3, 2012 doi:10.1152/ajpregu.00390.2012.-Insulin has long been hypothesized to cause sodium retention, potentially of enough magnitude to contribute to hypertension in obesity, metabolic syndrome, and Type II diabetes. There is an abundance of supportive evidence from correlational analyses in humans, acute insulin infusion studies in humans and animals, and chronic insulin infusion studies in rats. However, the absence of hypertension in human insulinoma patients, and negative results for sodium-retaining or blood pressure effects of chronic insulin infusion in a whole series of dog studies, strongly refute the insulin hypothesis. We recently questioned whether the euglycemic, hyperinsulinemia model used for most insulin infusion studies, including the previous chronic dog studies, was the most appropriate model to test the renal actions of insulin in obesity, metabolic syndrome, and Type II diabetes. In those circumstances, hyperinsulinemia coexists with hyperglycemia. Therefore, we tested the sodium-retaining effect of insulin in chronically instrumented, alloxan-treated diabetic dogs. We used 24 h/day intravenous insulin infusion to regulate plasma insulin concentration. Induction of diabetes (ϳ400 mg/dl) caused sustained natriuresis and diuresis. However, if we clamped insulin at baseline, control levels, i.e., prevented it from decreasing, then the sustained natriuresis and diuresis were completely reversed, despite the same level of hyperglycemia. We also found that 24 h/day intrarenal insulin infusion had the same effect in diabetic dogs but had no sodium-retaining action in normal dogs. This new evidence that insulin has a sodium-retaining effect during hyperglycemia may have implications for maintaining sodium balance in uncontrolled Type II diabetes.diabetes; insulin; diuresis; natriuresis; sodium balance RAISING THE QUESTION of whether insulin causes renal sodium retention, either in a scientific presentation or in the literature, immediately evokes one of two responses from the audience: 1) "I already know that insulin causes sodium retention", or 2) "Insulin does not cause sodium retention." Those maintaining the latter essentially have closed the book on the subject, and those holding to the former are interested in mechanisms but not the overarching question of whether insulin causes renal sodium retention. There is a wealth of literature to support both positions. However, nuances in many early studies raised issues that never were resolved. Inertia in the literature left many of those issues fading in the distance, all but erased from current thinking. We recently revisited the question about insulin and sodium retention, and our results were so striking that both positions on the subject warrant reconsideration. This review will chronologically present the literature supporting each position and show how our recent reports add new insigh...

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Section: Conclusion 1: Insulin Is a Sodium Retainermentioning

confidence: 99%

Sodium-retaining effect of insulin in diabetes

Brands¹,

Manhiani²

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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show abstract

“…Obese patients are more likely to have hypertension, due to a multifaceted pathophysiology involving insulin resistance and renal derangement among other factors (40). All patients are at risk for acute elevations in blood pressure during a procedure because of pain-induced sympathetic stimulation and recent discontinuation of oral antihypertensive medications.…”

Section: Hypertension Managementmentioning

confidence: 99%

Optimizing care for the obese patient in interventional radiology

Aberle

Charles

Hodak

et al. 2017

Diagn Interv Radiol

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“…CTRP1 stimulates aldosterone production through the induction of CYP11B2 gene expression [1]. Obesity and metabolic syndrome are frequently associated with elevated levels of aldosterone [7] and it is well known that obesity is the leading cause of hypertension [8,9]. Elevated aldosterone levels and expanded extracellular volume are key components of obesity-induced renal disease via aldosterone's non-epithelial effects on the kidney [7].…”

Section: Introductionmentioning

confidence: 99%