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Cholecystokinin octapeptide inhibits carotid sinus barorefiex in anesthetized rats

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Author:
No author available
Journal Title:
ACTA PHYSIOLOGICA SINICA
Issue:
1
DOI:
10.3321/j.issn:0371-0874.2004.01.005
Key Word:
八肽胆囊收缩素;丙谷胺;Bay K 8644;压力感受器反射;L-NAME;平均动脉压;cholecystokinin octapeptide (CCK-8);proglumide;Bay K 8644;baroreflex;L-NAME;mean arterial pressure

Abstract: The purpose of this study was to determine the effect of cholecystokinin octapeptide (CCK-8) on carotid sinus baroreflex in 36 anesthetized male rats by isolated carotid sinus perfusion in vivo. The results obtained are as follows. (1) By perfusion with CCK-8 (0.1, 0.5, 1.0 μmol/L), the functional curve of baroreflex was shifted to the right and upward, with a decrease in peak slope (PS) (P<0.001) and a reflex decrease (RD) in mean arterial pressure, while the threshold pressure (TP) and saturation pressure (SP) were significantly increased. Among the functional parameters of carotid sinus baroreflex, the changes in RD, PS and TP were dose-dependent. (2) Pretreatment with proglumide (100 μmol/L), a nonselective CCK receptor antagonist,the inhibitory effect of CCK-8 (0.5 μmol/L) on the baroreflex was significantly attenuated. (3) Pretreatment with L-NAME (100μmol/L), an inhibitor of nitric oxide (NO) synthase, did not affect the inhibitory action of CCK-8 (0.5 μmol/L). (4) Preperfusion with Bay K 8644 (500 nmol/L), an agonist of calcium channel, could attenuate the effect of CCK-8 (0.5 μmol/L). It is suggested that the inhibitory action of CCK-8 on the baroreflex may be mediated by the activation of its receptors in the carotid sinus baroreceptor, leading to an inhibition of stretch-sensitive channels and a decrease in Ca2+ influx. However, NO released from the endothelium seems not to be involved in the mechanism of this effect.

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