title: Cilnidipine improves spontaneously hypertensive rat coronary hemodynamics without altering cardiovascular mass and collagen.
abstract: OBJECTIVE
  The 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.
  
  
  METHODS
  Male 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.
  
  
  RESULTS
  The 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.
  
  
  CONCLUSIONS
  These 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.
authors.affiliation: Hypertension Research Laboratory, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121, USA.
authors.forename: Jasmina
authors.initials: J
authors.lastname: Varagic
authors.forename: Dinko
authors.initials: D
authors.lastname: Susic
authors.forename: Edward D
authors.initials: ED
authors.lastname: Frohlich
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002319:Cardiovascular System / Q000187:drug effects*; D003094:Collagen / Q000187:drug effects*; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology*; D004095:Dihydropyridines / Q000494:pharmacology*; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D008297:Male; D008955:Models, Cardiovascular; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D016276:Ventricular Function
chemical_list: D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D003094:Collagen; C065927:cilnidipine