Elsevier

Surgery for Obesity and Related Diseases

Volume 5, Issue 5, September–October 2009, Pages 615-620
Surgery for Obesity and Related Diseases

Review article
Bariatric surgery and hypertension

https://doi.org/10.1016/j.soard.2009.03.218Get rights and content

Section snippets

Mechanisms behind obesity-associated hypertension

Hypertension is associated with central adiposity and insulin resistance [8], [9]; however, the pathophysiologic basis remains unclear. Several hypotheses concerning the mechanisms for obesity-induced hypertension are plausible, including insulin resistance, aldosterone- and aldosterone-releasing factors (ARF), and leptin (Fig. 1).

Hypertension after bariatric surgery

Gastric bypass surgery is one of the most effective methods of obesity treatment, and the beneficial effects on obesity-related co-morbidities, such as hypertension, have been well documented [42], [43]. In the Swedish Obese Subjects study, systolic blood pressure decreased about 11 mm Hg and diastolic blood pressure 7 mm Hg in the first 6 months after bariatric surgery [44], [45]; however, the effect was not sustained in the long term. Several other studies have reported similar observations

Concept of “enterorenal axis”

The reduction of the visceral fat mass and subsequent decrease of sympathetic activation and sodium retention is not immediate and does not explain the early reductions in blood pressure after Roux-en-Y gastric bypass described by Ahmed et al. [51]. Thus, we hypothesized that gut hormones might be partly involved in the early resolution of hypertension after gastric bypass by a modification of the salt and water handling of the kidney. The idea that dietary intake and composition can affect

Potential candidate mediator between gut and kidney: GLP-1

Exogenous GLP-1 administered in animal studies had natriuretic and diuretic properties, and exendin-(9-39) amide, a GLP-1 antagonist, blocked natriuresis. In addition, intracerebroventricular administration of GLP-1-(7-36) amide inhibited food and water intake in rats [65], [66]. Furthermore, intracerebroventricular GLP-1 stimulated urinary excretion of water and sodium. The N-terminally extended and inactive, GLP-1-(1-36), did not exert natriuretic effects. Moreno et al. [67] investigated the

Conclusion

Hypertension is frequent in the obese and can have detrimental effects on the kidney and heart. Bariatric surgery can lead to significant improvement of salt-sensitive hypertension in obese subjects. Some evidence has shown that gut hormones might be involved in sodium and water handling in both animals and humans. Gut hormones might contribute to the improvement of hypertension after bariatric surgery. The underlying mechanisms require additional elucidation and could pave the way for future

Disclosures

Supported by the Deutsche Forschungsgemeinschaft. The authors claim no commercial associations that might be a conflict of interest in relation to this article.

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