Intestinal nitric oxide output during reduced mucosal blood flow in healthy volunteers

Snygg, Johan; Åneman, Anders; Pettersson, Anders; Fändriks, Lars

doi:10.1097/01.ccm.0000080489.67211.1f

Cited by 4 publications

(5 citation statements)

References 51 publications

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“…Chloroquine increases nitric oxide (NO) synthesis . NO could be produced by intestinal mucosa . NO inhibits small intestinal motility, especially tonic contraction .…”

Section: Resultsmentioning

confidence: 99%

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Relaxant effect of chloroquine in rat ileum: possible involvement of nitric oxide and BKCa

Jing

Liu

Yang

et al. 2013

Journal of Pharmacy and Pharmacology

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“…Chloroquine increases nitric oxide (NO) synthesis . NO could be produced by intestinal mucosa . NO inhibits small intestinal motility, especially tonic contraction .…”

Section: Resultsmentioning

confidence: 99%

“…It seems that CCK was not involved in the inhibitory effect of chloroquine on longitudinal muscle contraction. NO could be produced by intestinal mucosa . NO inhibits small intestinal motility, especially tonic contraction .…”

Section: Discussionmentioning

confidence: 99%

Relaxant effect of chloroquine in rat ileum: possible involvement of nitric oxide and BKCa

Jing

Liu

Yang

et al. 2013

Journal of Pharmacy and Pharmacology

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“…This splanchnic response has been shown to correlate with a markedly increased expression of Ang II . Furthermore, lower‐body negative pressure induction in normal human volunteers has also been shown to raise serum Ang II and reduce intestinal mucosal nitric oxide production …”

Section: Potential Clinical Implications Of Ras In Gastrointestinal Dmentioning

confidence: 94%

“…137 Furthermore, lower-body negative pressure induction in normal human volunteers has also been shown to raise serum Ang II and reduce intestinal mucosal nitric oxide production. 138 The administration of candesartan maintained jejunal and mucosal perfusion during severe hypovolaemia in pigs and reduced mortality. 139,140 A further porcine study reported improved mucosal oxygen delivery, but not an improvement in intestinal mucosal acidosis in pigs administered candesartan during endotoxic shock.…”

Section: Mesenteric Ischaemiamentioning

confidence: 99%

Review article: the pathophysiological roles of the renin–angiotensin system in the gastrointestinal tract

Garg

Angus

Burrell

et al. 2012

Aliment Pharmacol Ther

136

135

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Summary Background The renin‐angiotensin system (RAS) is a homeostatic pathway widely known to regulate cardiovascular and renal physiology; however, little is known about its influence in gastrointestinal tissues. Aim To elicit the anatomical distribution and physiological significance of the components of the RAS in the gastrointestinal tract. Methods An extensive online literature review including Pubmed and Medline. Results There is evidence for RAS involvement in gastrointestinal physiology and pathophysiology, with all the components required for autonomous regulation identified throughout the gastrointestinal tract. The RAS is implicated in the regulation of glucose, amino acid, fluid and electrolyte absorption and secretion, motility, inflammation, blood flow and possibly malignant disease within the gastrointestinal tract. Animal studies investigating the effects of RAS blockade in a range of conditions including inflammatory bowel disease, functional gut disorders, gastrointestinal malignancy and even intestinal ischaemia have been encouraging to date. Given the ready availability of drugs that modify the RAS and their excellent safety profile, an opportunity exists for investigation of their possible therapeutic role in a variety of human gastrointestinal diseases. Conclusions The gastrointestinal renin‐angiotensin system appears to be intricately involved in a number of physiological processes, and provides a possible target for novel investigative and therapeutic approaches.

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“…However, if longstanding, the hypoperfusive state will be associated with a general downregulation of GI functions, including also the barrier properties of the intestinal mucosa. 22,24 This, in turn, may be deleterious for the organism. Barrier dysfunction allows penetration of luminal microbiota and endotoxins into the intestinal tissue increasing the risk for induction of a systemic inflammatory response that in a worst case scenario affects distant organs resulting in multiple organ dysfunction and failure.…”

Section: Gi Circulationmentioning

confidence: 99%

The angiotensin II type 2 receptor and the gastrointestinal tract

Fändriks

2009

J Renin Angiotensin Aldosterone Syst

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The renin-angiotensin system (RAS) is well known for its vital involvement in body fluid homeostasis and circulation. However, very little research has been devoted to the impact of this regulatory system on the gastrointestinal (GI) system. This is surprising because the GI tract is fundamental for the intake and excretion of fluid and electrolytes (and nutrients), and it accommodates a large proportion of bodily haemodynamics and host defence systems. The RAS is well expressed and active in the GI tract, although the exact roles for the key mediator angiotensin II (Ang II) and its receptors in general, and the type 2 (AT 2 ) receptor in particular, are not completely settled. There are several reports showing Ang II regulation of intestinal fluid and electrolyte transport. For example, mucosaprotective duodenal bicarbonate-rich secretion is inhibited by Ang II via type 1 (AT 1 ) receptor-mediated facilitation of sympathoadrenergic activity, but this secretory process can also be stimulated by Ang II via AT 2 receptors. Novel data from human oesophagus and jejunum suggest that the AT 1 receptor mediates muscular contractions and that the AT 2 receptor regulates epithelial functions. Data are accumulating suggesting involvement of AT 1 and AT 2 receptors in GI inflammation and carcinogenesis. The picture of the RAS and AT 2 receptor in the GI tract is, however, far from complete. Much more basic research is needed with regard to GI pathophysiology before concluding clinical significance and potential applicability of pharmacological interferences with the RAS.

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Intestinal nitric oxide output during reduced mucosal blood flow in healthy volunteers

Abstract: Intestinal tonometry in humans exhibits a considerable mucosal nitric oxide formation that varies in relation to intestinal motility. Intestinal nitric oxide production is depressed during conditions with lowered mucosal blood perfusion.

Cited by 4 publications

References 51 publications

Relaxant effect of chloroquine in rat ileum: possible involvement of nitric oxide and BKCa

Relaxant effect of chloroquine in rat ileum: possible involvement of nitric oxide and BKCa

Review article: the pathophysiological roles of the renin–angiotensin system in the gastrointestinal tract

The angiotensin II type 2 receptor and the gastrointestinal tract

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