title: Coronary hemodynamics in aging spontaneously hypertensive and normotensive Wistar-Kyoto rats.
abstract: OBJECTIVE
  To delineate hypertension-related and age-related changes in coronary hemodynamics and to assess the role of myocardial (i.e. left ventricular) hypertrophy and cardiac fibrosis in inducing progressive deterioration of coronary flow reserve associated both with hypertension and with aging.
  
  
  METHODS
  Systemic and coronary hemodynamics (using radionuclide-labeled microspheres), right ventricular, left ventricular, and aortic mass indexes, and ventricular hydroxyproline concentrations (an estimate of collagen) in normotensive Wistar-Kyoto and spontaneously hypertensive rats aged 22, 35, and 65 weeks were determined.
  
  
  RESULTS
  Spontaneously hypertensive rats of all ages had greater left ventricular and aortic masses, greater collagen concentrations in both ventricles, a lower coronary flow reserve, and greater minimal coronary vascular resistance after administration of dipyridamole than did Wistar-Kyoto rats. Despite spontaneously hypertensive rats having only left ventricular hypertrophy, coronary hemodynamics were impaired to the same extent in both ventricles. Progressive increases in myocardial collagen concentration, decreases in coronary flow reserve, and increases in minimal coronary vascular resistance were observed in rats of both strains with aging. A positive correlation and linear regression between myocardial collagen concentration and minimal vascular resistance were found for both ventricles of rats of both strains.
  
  
  CONCLUSIONS
  Both aging and hypertension adversely affected the coronary circulation; furthermore, these effects appeared to be additive. Cardiac fibrosis, but not hypertrophy, might play a role in progressive deterioration of coronary hemodynamics in aging and hypertension and could provide an explanation for the diastolic dysfunction encountered clinically in older patients with hypertension.
authors.affiliation: Division of Research, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121, USA.
authors.forename: D
authors.initials: D
authors.lastname: Susic
authors.forename: E
authors.initials: E
authors.lastname: Nunez
authors.forename: K
authors.initials: K
authors.lastname: Hosoya
authors.forename: E D
authors.initials: ED
authors.lastname: Frohlich
mesh_terms: D000375:Aging / Q000473:pathology / Q000502:physiology; D000818:Animals; D001011:Aorta / Q000473:pathology; D001835:Body Weight; D003094:Collagen / Q000378:metabolism; D003326:Coronary Circulation / Q000502:physiology*; D005355:Fibrosis; D006439:Hemodynamics; D006909:Hydroxyproline / Q000378:metabolism; D006973:Hypertension / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014655:Vascular Resistance
chemical_list: D003094:Collagen; D006909:Hydroxyproline