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Cilnidipine improves spontaneously hypertensive rat coronary hemodynamics without altering cardiovascular mass and collagen

 

作者: Jasmina Varagic,   Dinko Susic,   Edward Frohlich,  

 

期刊: Journal of Hypertension  (OVID Available online 2002)
卷期: Volume 20, issue 2  

页码: 317-322

 

ISSN:0263-6352

 

年代: 2002

 

出版商: OVID

 

关键词: aortic and ventricular mass and fibrosis;calcium antagonist;spontaneously hypertensive rats;systemic and regional hemodynamics

 

数据来源: OVID

 

摘要:

ObjectiveThe present study was designed to determine the effects of prolonged treatment with cilnidipine, a novel dihydropyridine calcium antagonist which blocks both L-type and N-type calcium channels, on systemic, regional and coronary hemodynamics, cardiovascular mass and collagen content in normotensive Wistar–Kyoto (WKY) and spontaneously hypertensive (SHR) rats.MethodsMale 23-week-old WKY and SHR rats were divided into two groups for each strain. One group received cilnidipine (10 mg/kg per day), whereas their respective controls were given no therapy. Systemic and regional hemodynamics (radionuclide-labeled microspheres), left and right ventricular and aortic mass, and hydroxyproline concentration were determined after 12 weeks treatment.ResultsThe data demonstrated that cilnidipine neither affected systemic hemodynamics nor cardiovascular mass and collagen content in WKY rats. The same treatment in the SHR reduced arterial pressure and total peripheral resistance without changes in heart rate and cardiac index. Ventricular and aortic mass indices as well as ventricular collagen content remained unchanged. There were no differences in organ blood flows between two SHR groups, whereas renal, liver and left ventricular coronary vascular resistances were reduced by cilnidipine. After dipyridamole infusion left ventricular minimal coronary vascular resistance decreased further in cilnidipine-treated SHR as compared with control SHR rats.ConclusionThese data suggest that cilnidipine, an L- and N- type calcium channel antagonist, exerted beneficial effects on coronary hemodynamics without altering cardiovascular mass or collagen content in SHR.

 

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