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2005 | 56 | 3 |

Tytuł artykułu

ACE inhibitor and AT1 antagonist stimulate duodenal HCO3 secretion mediated by a common pathway - involvement of PG, NO and bradykinin

Treść / Zawartość

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Recent study demonstrated that duodenal HCO3- secretion is affected by modulation of the renin-angiotensin system. We examined the effects of enalapril (angiotensin-converting enzyme (ACE) inhibitor) or losartan (angiotensin AT1 receptor antagonist) on duodenal HCO3- secretion in rats and investigated the mechanisms involved in the renin-angiotensin system-related HCO3- response. A proximal duodenal loop was perfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist). Although losartan alone did not affect the HCO3- secretion, despite reducing MBP, the agent dose-dependently increased the HCO3- secretion in the presence of angiotensin II, and this response was totally antagonized by prior administration of FR172357, indomethacin and L-NAME. Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357. Both prostaglandin (PG) E2 and the nitric oxide (NO) donor NOR-3 also increased the HCO3- secretion, the latter effect being inhibited by indomethacin. These results suggest that both an ACE inhibitor and AT1 antagonist (in the presence of angiotensin II) increase duodenal HCO3- secretion via a common pathway, involving bradykinin, NO and PGs. It is also assumed that bradykinin releases NO locally, which in turns stimulates HCO3- secretion mediated by PGs.

Wydawca

-

Rocznik

Tom

56

Numer

3

Opis fizyczny

p.391-406,fig.,ref.

Twórcy

autor
  • Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto 607, Japan
autor
autor
autor

Bibliografia

Typ dokumentu

Bibliografia

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bwmeta1.element.agro-article-437dd846-ca26-4feb-b39a-fd938086c2ae
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