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Title: The interaction of cholecystokinin and its fragments with norepinephrine in the circulatory system of diabetic rats. Author: Fiedorowicz RJ, Wiśniewski K. Journal: Pol J Pharmacol Pharm; 1989; 41(6):573-83. PubMed ID: 2577226. Abstract: The interaction of cholecystokinin (CCK-33) and its fragments, C-terminal octapeptide (CCK-8) and C-terminal tetrapeptide (CCK-4) with norepinephrine (NE) was studied in rats with streptozotocin (STZ)-induced diabetes. The rats, male Wistar, were divided into three groups: control, diabetic and insulin-treated diabetic. Twenty-eight days after STZ administration, the systolic and diastolic arterial blood pressure, heart rate and the function of the heart isolated by the Langendorff method were studied. NE caused a rise in systolic blood pressure in the control and insulin-treated diabetic rats, the opposite effect of NE was observed in diabetic rats. NE had no effect on heart rate in any of the groups studied. CCK-33 potentiated the hypertensive effect of NE in the control rats reduced the hypertensive effect of this amine in diabetic rats treated with insulin and its hypotensive effect in the diabetic rats. CCK-8 did not change the NE effect on arterial blood pressure in the control and insulin-treated diabetic rats but did reduce the hypotension caused by NE in diabetic rats. CCK-4 did not change the effects of NE in any of the groups. NE induced an increase in cardiac contraction amplitude in all rats but its positive inotropic action was found to be the weakest in the diabetic rats. Administration of CCK-33 did not change the positive inotropic effect of NE in any of the groups but did, however, weaken its influence on heart rate in diabetic rats and insulin-treated diabetic rats. CCK-8 reduced the positive inotropic action of NE but did not affect its chronotropic effect. CCK-4 had no effect on the action of NE in any of the groups. Diabetes can change the response of alpha-adrenergic system to CCK-33 and NE. Insulin partially normalized the circulatory system response in the diabetic rats.[Abstract] [Full Text] [Related] [New Search]