title: Equipotent antihypertensive agents variously affect pulsatile hemodynamics and regression of cardiac hypertrophy in spontaneously hypertensive rats.
abstract: BACKGROUND
  Converting enzyme inhibitors are more effective than arteriolar vasodilators at regressing left ventricular hypertrophy in spontaneously hypertensive rats (SHR), possibly because of nonhemodynamic factors. However, the pulsatile component of hemodynamic load has not been evaluated in this model.
  
  
  RESULTS
  We measured pulsatile hemodynamics in 18-month-old male SHR after 6 months of therapy with either zofenopril (Z), hydralazine (H), or water (W). Hydralazine and zofenopril reduced mean arterial pressure comparably (W, 106 +/- 23 versus H, 81 +/- 12 versus Z, 84 +/- 18 mm Hg, P = .002) yet had a differential effect on the ratio of left ventricular weight to body weight (W, 3.9 +/- 0.5 versus H, 3.3 +/- 0.4 versus Z, 2.4 +/- 0.2 g/kg, P < .005). Hydralazine-treated SHR had increased characteristic impedance (P = .0011) and a persistently low ratio of the reflected-wave transit time to left ventricular ejection time (P < .001), which contributed to early and late systolic loading, respectively, of the left ventricle. Consequently, only zofenopril-treated SHR had a significant reduction in left ventricular systolic force-time integral (P = .02), a measure of total ventricular load. There were no differences in systolic stress-time integral, suggesting that mass was appropriate to load when all elements of steady-flow and pulsatile load were considered.
  
  
  CONCLUSIONS
  A blunted reduction in total left ventricular load, due to increased pulsatile load in SHR treated with hydralazine, provided a hemodynamic basis for the differential regression of hypertrophy in this model of genetic hypertension.
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115, USA. gfmitchell@bics.bwh.harvard.edu
authors.forename: G F
authors.initials: GF
authors.lastname: Mitchell
authors.forename: M A
authors.initials: MA
authors.lastname: Pfeffer
authors.forename: P V
authors.initials: PV
authors.lastname: Finn
authors.forename: J M
authors.initials: JM
authors.lastname: Pfeffer
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D002216:Captopril / Q000031:analogs & derivatives / Q000494:pharmacology; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects*; D006830:Hydralazine / Q000494:pharmacology; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D008297:Male; D011673:Pulsatile Flow / Q000187:drug effects; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011919:Rats, Inbred Strains; D012074:Remission Induction; D016277:Ventricular Function, Left / Q000187:drug effects; D014867:Water / Q000494:pharmacology
chemical_list: D000959:Antihypertensive Agents; D014867:Water; D006830:Hydralazine; C044958:zofenopril; D002216:Captopril