Cardiovascular actions of the calmodulin inhibitor felodipine
Autor: | Pieter D. Verdouw, M. G. Scheffer, Bruce H. R. Wolffenbuttel |
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Rok vydání: | 1983 |
Předmět: |
medicine.medical_specialty
Cardiac output Nifedipine Swine Hemodynamics Coronary circulation Oxygen Consumption Calmodulin Afterload Coronary Circulation Internal medicine medicine Animals Antihypertensive Agents Pharmacology Felodipine business.industry Myocardium Heart General Medicine Blood flow medicine.anatomical_structure Blood pressure Anesthesia Injections Intravenous Cardiology business medicine.drug |
Zdroj: | Naunyn-Schmiedeberg's Archives of Pharmacology. 323:350-354 |
ISSN: | 1432-1912 0028-1298 |
DOI: | 10.1007/bf00512475 |
Popis: | The cardiovascular effects of intravenous (1.5-10 nmol X kg-1) and intracoronary (50 nmol) administration of felodipine, 4-(2,3-dichlorophenyl)-1,4-dihydro-2, 6-dimethyl-3-ethoxycarbonyl-5-methoxycarbonylpyridine, were studied in anaesthetized pigs. Following intravenous administration dose-dependent decreases were observed in left ventricular systolic blood pressure (up to 30%) and in the resistances of the systemic (up to 40%) and coronary vascular beds (up to 45%), whereas heart rate, cardiac output, myocardial contractility (regional and global), and left ventricular end-diastolic pressure were minimally affected. Myocardial blood flow increased independently of the dose (20%), while the coronary venous O2-content more than doubled. The concomitant decrease in myocardial O2-consumption (up to 30%) was dose-dependent in the range from 1.5-6.75 nmol X kg-1. Intracoronary administration of 50 nmol had only minor effects on global and regional myocardial performance but produced a doubling of the coronary blood flow which was accompanied by a 70% decrease in myocardial O2-extraction. O2-consumption decreased considerably more (35%) than after intravenous administration in spite of the minimal decrease in O2-demand (7%). We conclude that felodipine dilates both systemic and coronary blood vessels. Although the reduction in myocardial O2-consumption is primarily caused by the reduction in afterload, a direct effect on myocardial metabolism can also be involved. |
Databáze: | OpenAIRE |
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