title: Lisinopril reduces left ventricular hypertrophy and cardiac polyamine concentrations without a reduction in left ventricular wall stress in transgenic Tsukuba hypertensive mice.
abstract: This experiment was designed to determine how the angiotensin-converting enzyme inhibitor, lisinopril, acts on left ventricular wall stress and cardiac polyamine concentrations in Tsukuba hypertensive mice (THMs) carrying both human renin and angiotensinogen genes. Twelve-week-old THMs were treated with either lisinopril or hydralazine, or were left untreated, for 8 weeks. C57BL/6 mice of similar age were used as normal controls. Each group consisted of 14 mice. The systolic blood pressure of each mouse was measured once a week. Mice were euthanized at 20 weeks of age, and the left ventricular weight, left ventricular diameter, left ventricular wall stress, and left ventricular polyamine concentrations were measured. The systolic blood pressure of the untreated group was approximately 35 mmHg higher than that of the C57BL/6 mice. The left ventricular weight, left ventricular diameter, left ventricular wall stress, and left ventricular polyamine concentrations in the untreated group were significantly higher compared to those in the C57BL/6 mice. The lisinopril group had significantly decreased systolic blood pressure and other measurement items, except the left ventricular wall stress, in comparison with the untreated group. The hydralazine group also had significantly decreased systolic blood pressure and left ventricular wall stress when compared with the untreated group, but no significant differences in other measurement items when compared with the untreated group. These findings indicate that lisinopril reduces left ventricular hypertrophy and polyamine concentration without reducing left ventricular wall stress, and that simply decreasing blood pressure does not suppress left ventricular hypertrophy.
authors.affiliation: First Department of Internal Medicine, Kinki University School of Medicine, Osakasayama, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kai
authors.forename: K
authors.initials: K
authors.lastname: Ishikawa
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D006830:Hydralazine / Q000494:pharmacology; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology*; D017706:Lisinopril / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D009994:Osmolar Concentration; D011073:Polyamines / Q000037:antagonists & inhibitors*; D012016:Reference Values; D013314:Stress, Mechanical; D013599:Systole; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D011073:Polyamines; D006830:Hydralazine; D017706:Lisinopril