Wiśniewska R J, Wiśniewski K
Department of Pharmacology, Bialystok Medical Academy, Poland.
Pol J Pharmacol. 1996 May-Jun;48(3):293-7.
The interaction of C-terminal cholecystokinin octapeptide (CCK-8) with beta-adrenoceptors agonist (isoprenaline-ISO) and antagonist (propranolol) and their influence on arterial blood pressure and function of isolated heart in rats with streptozotocin-induced diabetes mellitus (DM) was studied. After blockade of beta-adrenoceptors with propranolol, the hypertensive effect of CCK-8 was observed in the control group but not in DM-group, whereas CCK-8 had no effect on arterial blood pressure in the both studied groups. Stimulation of beta-adrenoceptors with ISO exerted the hypotensive effect of CCK-8 similar as after administration of the amine alone in the control and diabetic rats. CCK-8 increased the cardiac contraction amplitude and had no effect on heart rate and coronary outflow in control hearts. The positive inotropic effect of the peptide was abolished in DM-group. After blockade of beta-adrenoceptors, CCK-8 decreased all studied parameters of isolated hearts, the effect was similar as after infusion of propranolol alone. In DM group, after blockade of beta-adrenoceptors CCK-8 evoked decrease in the cardiac contraction amplitude (as during infusion of propranolol) and heart rate (the effect was greater than that after beta-adrenoceptors antagonist). CCK-8 administrated with ISO increased amplitude, heart rate and decreased coronary outflow of isolated control heart as after administration of ISO alone: in DM-group only the positive inotropic effect was observed. DM modified the effect of CCK-8 in circulatory system of rats. CCK-8 evoked bradycardia independent of stimulation or blockade of beta-adrenoceptors, mainly in DM.
研究了C端胆囊收缩素八肽（CCK-8）与β-肾上腺素能受体激动剂（异丙肾上腺素-ISO）和拮抗剂（普萘洛尔）的相互作用，以及它们对链脲佐菌素诱导的糖尿病（DM）大鼠动脉血压和离体心脏功能的影响。用普萘洛尔阻断β-肾上腺素能受体后，在对照组中观察到CCK-8的升压作用，而在糖尿病组中未观察到，而CCK-8对两个研究组的动脉血压均无影响。用ISO刺激β-肾上腺素能受体后，CCK-8产生的降压作用与单独给予该胺后在对照大鼠和糖尿病大鼠中产生的降压作用相似。CCK-8增加了对照心脏的心肌收缩幅度，对心率和冠脉流量无影响。在糖尿病组中，该肽的正性肌力作用消失。阻断β-肾上腺素能受体后，CCK-8降低了离体心脏的所有研究参数，其作用与单独输注普萘洛尔后的作用相似。在糖尿病组中，阻断β-肾上腺素能受体后，CCK-8引起心肌收缩幅度降低（与输注普萘洛尔时一样）和心率降低（该作用大于β-肾上腺素能受体拮抗剂给药后的作用）。与ISO一起给予CCK-8时，离体对照心脏的幅度、心率增加，冠脉流量降低，与单独给予ISO后一样：在糖尿病组中仅观察到正性肌力作用。糖尿病改变了CCK-8在大鼠循环系统中的作用。CCK-8引起心动过缓，与β-肾上腺素能受体的刺激或阻断无关，主要发生在糖尿病大鼠中。
