[Effect of enalapril on heart rate, arterial blood pressure and exocrine pancreatic secretion in the alert dog].

A changed exocrine pancreatic secretion could be a pathogenetic factor of an acute pancreatitis after administration of angiotensin-converting enzyme (ace) inhibitors. In six conscious dogs with gastric and duodenal Thomas fistulas we studied the effect of an intravenous (iv.) bolus injection of 10 mg enalaprilat, an intraduodenal (id.) bolus injection of 20 and 40 mg enalapril (e.), and 0.15 M NaCl (20 ml iv., resp., id.) on pancreatic bicarbonate- and protein output in response to secretin (20.5 pmol/kg bw/h and caerulein (29.6 pmol/kg bw/h). Arterial blood pressure and heart rate we also measured. The iv. and id. injection of enalapril(at) significantly increased heart rate by 28% after 10 mg of e. iv. [peak 101 +/- 11 beats/min, N = 6, X +/- SEM] and by 13 resp. 37% after 20 resp. 40 mg e. id. [peak 89 +/- 4, resp., 108 +/- 7 beats/min] as compared to control [peak 79 +/- 5 beats/min]. Systolic blood pressure was significantly decreased by 6% after 10 mg e. iv. [lowest value 121 +/- 2 mm Hg] and by 8% and 9% after 20 and 40 mg e. id., respectively, [lowest value 119 +/- 2, resp., 118 +/- 1 mm Hg] as compared to control [lowest value 129 +/- 1 mm Hg]. The applied enalapril(at) doses had no significant effect on hormonal stimulated pancreatic bicarbonate- and protein output. The results confirmed the well known effects of enalapril(at) on heart rate and on arterial blood pressure. Beyond that the results exposed that therapeutical doses of enalapril(at) had no significant effect on exocrine pancreatic secretion. Conclusion of this study is that a pathogenetic role of pancreatic exocrine secretion in the ace-inhibitors and the acute pancreatitis induced by ace-inhibitors is unlikely.