Angiotensin II induces apoptosis in intestinal epithelial cells through the AT2 receptor, GATA-6 and the Bax pathway

Sun, Lihua; Wang, Wensheng; Xiao, Weidong; Liang, Hongyin; Yang, Yang; Yang, Hua

doi:10.1016/j.bbrc.2012.07.003

Cited by 46 publications

(36 citation statements)

References 41 publications

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“…ANGII induced apoptosis of IECs, and it was inhibited by AT1R inhibitor. Interestingly, in our previous study, we had also found that AT2R blockage diminished the ANGIIinduced elevation of apoptosis in cultured Caco-2 cell lines (27). Apoptosis is controlled in part by a complex interplay between regulatory proteins such as proapoptotic and anti-apoptotic mediators Bax and Bcl-2, respectively (30).…”

Section: Discussionmentioning

confidence: 94%

Essential Role of Angiotensin Receptors in the Modulation of Intestinal Epithelial Cell Apoptosis

Wang

Sun²,

Xiao³

et al. 2013

J. pediatr. gastroenterol. nutr.

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Section: Discussionmentioning

confidence: 94%

Essential Role of Angiotensin Receptors in the Modulation of Intestinal Epithelial Cell Apoptosis

Wang

Sun²,

Xiao³

et al. 2013

J. pediatr. gastroenterol. nutr.

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“…Ang II stimulates apoptosis in intestinal epithelial cells via the AT 2 receptor61. Activation of AT 2 by CGP-42112a causes increased nitric oxide production in jejunal mucosa62.…”

Section: Discussionmentioning

confidence: 99%

Dietary Sodium Suppresses Digestive Efficiency via the Renin-Angiotensin System

Weidemann

Voong

Morales-Santiago

et al. 2015

Sci Rep

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Dietary fats and sodium are both palatable and are hypothesized to synergistically contribute to ingestive behavior and thereby obesity. Contrary to this hypothesis, C57BL/6J mice fed a 45% high fat diet exhibited weight gain that was inhibited by increased dietary sodium content. This suppressive effect of dietary sodium upon weight gain was mediated specifically through a reduction in digestive efficiency, with no effects on food intake behavior, physical activity, or resting metabolism. Replacement of circulating angiotensin II levels reversed the effects of high dietary sodium to suppress digestive efficiency. While the AT1 receptor antagonist losartan had no effect in mice fed low sodium, the AT2 receptor antagonist PD-123,319 suppressed digestive efficiency. Correspondingly, genetic deletion of the AT2 receptor in FVB/NCrl mice resulted in suppressed digestive efficiency even on a standard chow diet. Together these data underscore the importance of digestive efficiency in the pathogenesis of obesity, and implicate dietary sodium, the renin-angiotensin system, and the AT2 receptor in the control of digestive efficiency regardless of mouse strain or macronutrient composition of the diet. These findings highlight the need for greater understanding of nutrient absorption control physiology, and prompt more uniform assessment of digestive efficiency in animal studies of energy balance.

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“…83,84 This may relate to the possibility that AT 2 receptor stimulation affects the incidence of myocardial infarction 85,86 and induces apoptosis in intestinal epithelial cells, thereby inducing severe gastrointestinal problems. 87,88 Additionally, AT 2 receptor stimulation activates the bradykinin axis, 89 although bradykinin accumulation will also occur after ACE inhibition. The exact contribution of bradykinin to the beneficial effects of RAAS blockade in humans remains to be determined.…”

Section: Desired Degree Of Raas Blockadementioning

confidence: 99%

Hypertension

Riet

Esch

Roks

et al. 2015

Circulation Research

570

251

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Blockers of the renin–angiotensin–aldosterone system (RAAS), that is, renin inhibitors, angiotensin (Ang)-converting enzyme (ACE) inhibitors, Ang II type 1 receptor antagonists, and mineralocorticoid receptor antagonists, are a cornerstone in the treatment of hypertension. How exactly they exert their effect, in particular in patients with low circulating RAAS activity, also taking into consideration the so-called Ang II/aldosterone escape that often occurs after initial blockade, is still incompletely understood. Multiple studies have tried to find parameters that predict the response to RAAS blockade, allowing a personalized treatment approach. Consequently, the question should now be answered on what basis (eg, sex, ethnicity, age, salt intake, baseline renin, ACE or aldosterone, and genetic variance) a RAAS blocker can be chosen to treat an individual patient. Are all blockers equal? Does optimal blockade imply maximum RAAS blockade, for example, by combining ≥2 RAAS blockers or by simply increasing the dose of 1 blocker? Exciting recent investigations reveal a range of unanticipated extrarenal effects of aldosterone, as well as a detailed insight in the genetic causes of primary aldosteronism, and mineralocorticoid receptor blockers have now become an important treatment option for resistant hypertension. Finally, apart from the deleterious ACE-Ang II-Ang II type 1 receptor arm, animal studies support the existence of protective aminopeptidase A-Ang III-Ang II type 2 receptor and ACE2-Ang-(1 to 7)-Mas receptor arms, paving the way for multiple new treatment options. This review provides an update about all these aspects, critically discussing the many controversies and allowing the reader to obtain a full understanding of what we currently know about RAAS alterations in hypertension.

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Angiotensin II induces apoptosis in intestinal epithelial cells through the AT2 receptor, GATA-6 and the Bax pathway

Cited by 46 publications

References 41 publications

Essential Role of Angiotensin Receptors in the Modulation of Intestinal Epithelial Cell Apoptosis

Essential Role of Angiotensin Receptors in the Modulation of Intestinal Epithelial Cell Apoptosis

Dietary Sodium Suppresses Digestive Efficiency via the Renin-Angiotensin System

Hypertension

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