title: Enhanced Ca2+-induced contractions and attenuated alpha-adrenoceptor responses in resistance arteries from rats with congestive heart failure.
abstract: OBJECTIVE
  The aim of the present study was to examine the role of Ca2+-mediated contractile responses in isolated mesenteric resistance arteries from rats with congestive heart failure (CHF).
  
  
  METHODS
  Heart failure was induced by ligation of the left coronary artery. Rats exposed to the same surgical procedure except ligation served as controls (Sham). The following experiments were conducted: (1) passive increase in radial stretch (the length-tension relationship) in Ca2+-free and in depolarizing high K+-solution; (2) the contractile responses to external application of Ca2+ and high K+-solutions in the presence of nifedipine and phentolamine; and (3) a histological evaluation of CHF and Sham vessels.
  
  
  RESULTS
  The length-tension induced response in Ca2+-free buffer solution was significantly lower in arteries from CHF rats, starting at a very low tension (0.9+/-0.2 mN/mm for heart failure and 1.7+/-0.2 mN/mm for Sham). This difference, but at a higher degree of stretch, was also present in K+-activated vessels. The external application of Ca2+ in K+-depolarized vascular segments in the presence of phentolamine (1 microM) induced an enhanced contractile response in arteries from CHF rats compared with Sham (4.8+/-0.3 mN/mm and 3.6+/-0.6 mN/mm, respectively, P=0.059). In the absence of phentolamine the reverse response was found (4.0+/-0.4 mN/mm and 5.7+/-0.3 mN/mm for CHF vs. Sham respectively, P=0.035). Application of increasing concentrations of K+-solution induced a stronger contractile response in Sham compared with CHF arteries (Sham 4.9+/-0.4 and heart failure 4.0+/-0.3, P=0.04). Microscopic examination of vessels yielded no difference in gross morphology, media thickness or wall to lumen ratio between CHF and Sham arteries.
  
  
  CONCLUSIONS
  The results indicate an attenuation of alpha-adrenoceptors and a difference of Ca2+-mediated vascular contractility in resistance arteries of congestive heart failure rats.
authors.affiliation: Department of Internal Medicine, Lund University, Lund, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Bergdahl
authors.forename: S
authors.initials: S
authors.lastname: Valdemarsson
authors.forename: X Y
authors.initials: XY
authors.lastname: Sun
authors.forename: T
authors.initials: T
authors.lastname: Hedner
authors.forename: L
authors.initials: L
authors.lastname: Edvinsson
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology*; D008297:Male; D008638:Mesenteric Arteries / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D009543:Nifedipine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011188:Potassium / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D018709:Statistics, Nonparametric; D014661:Vasoconstriction / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D018341:Receptors, Adrenergic, alpha-2; D014665:Vasodilator Agents; D009543:Nifedipine; D011188:Potassium; D002118:Calcium; D010646:Phentolamine