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The human duodenal mucosa harbors all components for a local renin angiotensin system.

Artikel i vetenskaplig tidskrift
Författare Emma Spak
Peter Hallersund
Anders Edebo
Anna Casselbrant
Lars Fändriks
Publicerad i Clinical science (London, England : 1979)
Volym 133
Nummer/häfte 8
Sidor 971-982
ISSN 1470-8736
Publiceringsår 2019
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för gastrokirurgisk forskning och utbildning
Sidor 971-982
Språk en
Länkar dx.doi.org/10.1042/CS20180877
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämneskategorier Medicinska grundvetenskaper

Sammanfattning

The renin-angiotensin system (RAS) is present in the gastrointestinal (GI) tract but remains to be fully characterized, particularly in man. The duodenum plays a role in both the upper and lower GI regulation, as well as in distant organs. The present study investigates the presence and functional potential of RAS in the human duodenal mucosa of healthy individuals. Endoscopically acquired mucosal biopsies from healthy volunteers were examined using western blot, immunohistochemistry, and ELISA. Functionality was examined by using Ussing chambers and recording duodenal transmucosal potential difference (PD) and motility in vivo Angiotensinogen, Angiotensin II (AngII) and its receptors (AT1R, AT2R) as well as to the RAS associated enzymes renin, ACE, and neprylisin were detected in all samples of duodenal mucosa. Migrating motility complex induced elevations of transmucosal PD were significantly larger after per-oral administration of the AT1R receptor antagonist candesartan. Fasting duodenal motility per se was not influenced by candesartan. The epithelial current produced by duodenal mucosae mounted in Ussing chambers increased significantly after addition of AngII to specimens where the AT1R was blocked using losartan. The epithelial current also increased after addition of the AT2R-selective agonist C21. Immunostaining and pharmacological data demonstrate the presence of a local RAS in the human duodenal mucosa with capacity to influence epithelial ion transport by way of particulary the AT2R.

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