Abstract
A transient significant decrease in mean arterial blood pressure (MAP) from 107 +/- 3 to 98 +/- 3 mmHg (P < 0.05) was observed in elderly (59-69 years of age), healthy volunteers 25-30 min following ingestion of a test meal. In young volunteers (22-34 years of age), a postprandial decrease of MAP from 88 +/- 3 to 83 +/- 4 mmHg was also noted but it was not statistically significant. A 40% decrease in bradykinin (BK) content of circulatory high molecular weight kininogen had previously been observed in human subjects given the same test meal. We presently demonstrate by specific ELISA that the stable pentapeptide metabolite (1-5 BK) of BK increases from 2.5 +/- 1.0 to 11.0 +/- 2.5 pg/ml plasma (P < 0.05) in elderly volunteers and from 2.0 +/- 1.0 to 10.3 +/- 3.2 pg/ml plasma (P < 0.05) in young volunteers 3 h following food intake. This result suggests that ingestion of food stimulates BK release from kininogen in normal man. Postprandial splanchnic vasodilatation, demonstrated by a decrease of plasma half-life of intravenously administered indocyanine green (ICG), a marker of mesenteric blood flow to the liver, from 4.4 +/- 0.4 to 3.0 +/- 0.1 min (P < 0.05) in young volunteers and from 5.2 +/- 1.0 to 4.0 +/- 0.5 min (P < 0.05) in elderly volunteers, accompanied BK release. The participation of BK in this response was investigated in subjects given the BK-potentiating drug captopril prior to food intake. Postprandial decreases of ICG half-lives were not changed by this treatment in either young or elderly subjects, a result which may indicate that BK released following food intake plays no role in postprandial splanchnic vasodilatation in normal man.
Highlights
Bradykinin (BK) modulates vascular tone as a direct effect and as a stimulant of nitric oxide release from the vascular endothelium
BK content of high molecular weight kininogen (HMWK) in plasma is decreased following food intake in healthy volunteers [2,3], suggesting that BK released by alimentary stimulation may contribute to postprandial hypotension by causing vasodilatation at the splanchnic level [3]
Postprandial BK release was studied by measuring by specific enzyme-linked immunosorbent assay (ELISA) the circulating amounts of the 1-5 BK pentapeptide, a metabolic product considerably more stable than BK [4,5], following ingestion of a test meal by healthy volunteers
Summary
Bradykinin (BK) modulates vascular tone as a direct effect and as a stimulant of nitric oxide release from the vascular endothelium. BK content of high molecular weight kininogen (HMWK) in plasma is decreased following food intake in healthy volunteers [2,3], suggesting that BK released by alimentary stimulation may contribute to postprandial hypotension by causing vasodilatation at the splanchnic level [3]. The measurement of changes in the circulatory half-life (t1/2) of intravenously administered indocyanine (cardio)-green (ICG), a dye which is fully and rapidly taken up by the liver, offers a simple and reliable means of assessing splanchnic (mostly mesenteric + hepatic) blood flow [6,7]. In order to test the hypothesis that BK contributes to postprandial splanchnic vascular changes, ICG was employed to determine whether the BKpotentiating drug captopril potentiates the decrease in splanchnic blood flow evoked by food intake
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