Enhanced contractility of the rat stomach during suppression of angiotensin converting enzyme by captopril in vitro

Abstract

1 Intragastric pressure (IGP) was used as an index, of the effect of serosal application of captopril (SQ 14,225; D-3-mercapto-2-methylpropanoyl-L-proline) on the contractility of rat stomach in vitro. 2 Captopril, at concentrations > 0.3 pm, enhanced the spontaneous gastric motility (GM) in a concentration-dependent manner whereas concentrations <0.3 pM selectively potentiated 4 nm bradykinin (BK)evoked gastric contractions without significantly affecting the spontaneous GM. 3 The kallikrein inhibitor, aprotinin (100uml-1), markedly antagonized the enhanced GM to 1.4pum captopril and BK (4nM)-evoked contractions, without affecting the contractions evoked by angiotensin 1 (10 nM) and acetylcholine (0.4pM). The angiotensin II antagonist, saralasin (50 pM) failed to mimic aprotinin. 4 The enhanced GM to captopril was markedly inhibited by tetrodotoxin (1 pM), and partially inhibited by atropine (1 pM).5 These results indicate that in vitro, captopril (> 0.3 pM) enhances gastric contractility through kininase/ ACE inhibitory action, presumably by increasing the concentration of undegraded tissue kinins and substance P. This motor response seems to be predominantly due to activation of the cholinergic neurones but non-cholinergic excitatory neurones are also involved.

Influence of acid suppressants on gastric emptying: Cross‐over analysis in healthy volunteers

“…They did not receive any medications such as gastrointestinal prokinetic agents, calcium antagonists, tricyclics, narcotics or selective serotonin reuptake inhibitors before or during the test period. Angiotensin‐converting enzyme inhibitor users were also excluded from the present study because this inhibitor has also been reported to influence gastric and esophageal motility 19,20 . Their lifestyle was unchanged during the test period, although there was no alcohol intake within 1 day before every examination.…”