Effects of cholecystokinin octapeptide on rat cardiac function and the receptor mechanism.
- Author:
Xiao-Yun ZHAO
1
;
Yi-Ling LING
;
Ai-Hong MENG
;
Bao-En SHAN
;
Jun-Lan ZHANG
Author Information
1. Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China. lingyiling@163.net
- Publication Type:Journal Article
- MeSH:
Animals;
Dose-Response Relationship, Drug;
Heart Rate;
drug effects;
Male;
Myocardium;
metabolism;
Rats;
Rats, Sprague-Dawley;
Receptors, Cholecystokinin;
drug effects;
Sincalide;
administration & dosage;
pharmacology;
Ventricular Function, Left;
drug effects;
Ventricular Pressure;
drug effects
- From:
Acta Physiologica Sinica
2002;54(3):239-243
- CountryChina
- Language:English
-
Abstract:
The aim of this study was to explore the effects of cholecystokinin octapeptide (CCK-8) on cardiac function and the receptor mechanism in anesthetized rats. The mean arterial pressure (MAP), heart rate (HR), the left ventricle systolic pressure (LVP) and the maximal/minimum rate of LVP (+/-LV dp/dt(max)) were measured. The results obtained are as follows. (1) Low dose of CCK-8 (0. 4 microgram/kg i.v.) caused tachycardia and slight increase in MAP, LVP and LV dp/dt(max) (P<0.01), while medium dose (4.0 microgram/kg i.v.) and high dose of CCK-8 (40 microgram/kg i.v.) elicited a bradycardia and marked increase in MAP, LVP and LV dp/dtmax (P<0.01). (2) Proglumide (1.0 mg/kg i.v.), a CCK-receptor (CCK-R) antagonist, significantly inhibited the pressor effects of CCK-8, whilst it reversed the bradycardic responses (P<0.01). (3) Using reverse transcription polymerase chain reaction (RT-PCR), CCK-A receptor (CCK-AR) and CCK-B receptor (CCK-BR) mRNA were expressed in myocardium of rats. The above results indicate that CCK-8 may enhance cardiac function in a dose-dependent manner and elicit a change in HR, which is likely induced by the activation of CCK-R on myocardium.
