Marker J D, Roberts M L
Department of Physiology, University of Adelaide, S.A.
Regul Pept. 1988 Mar;20(3):251-9. doi: 10.1016/0167-0115(88)90081-x.
Cholecystokinin octapeptide (CCK-8) administered i.v. to urethane-anaesthetized rats or added to the perfusion stream of isolated rat hearts produced an immediate bradycardia. The size of this response was dose-related. Studies in vivo and in vitro using atropine and propranolol indicated that the response to CCK-8 was largely due to a direct action of the peptide on the heart. N-carbobenzoxy-tryptophan (CBZ-Trp), a cholecystokinin receptor antagonist, abolished the response of the isolated heart to CCK-8. Gastrin I did not produce bradycardia. The receptors on rat heart were similar to the classes of cholecystokinin receptors found in brain and exocrine pancreas in that CCK-8 rather than cholecystokinin tetrapeptide (CCK-4) was the preferred agonist.
静脉注射给氨基甲酸乙酯麻醉的大鼠八肽胆囊收缩素（CCK - 8）或添加到离体大鼠心脏的灌注液中会立即引起心动过缓。这种反应的大小与剂量相关。体内和体外使用阿托品和普萘洛尔的研究表明，对CCK - 8的反应很大程度上是由于该肽对心脏的直接作用。N - 苄氧羰基 - 色氨酸（CBZ - Trp），一种胆囊收缩素受体拮抗剂，消除了离体心脏对CCK - 8的反应。胃泌素I不会引起心动过缓。大鼠心脏上的受体与在脑和外分泌胰腺中发现的胆囊收缩素受体类型相似，因为CCK - 8而非四肽胆囊收缩素（CCK - 4）是首选激动剂。
