title: Augmented responses of angiotensin I and II in patients with ischemic heart disease: relation to left ventricular function.
abstract: To evaluate the effects of left ventricular (LV) dysfunction upon the sympathetic nervous and renin-aldosterone-angiotensin systems, neurohormonal factors were measured in patients with ischemic heart disease. Eleven patients were divided into two groups by their LV ejection fraction based on previous catheterization; preserved (EF > or = 60%) and impaired (EF < 60%) LV systolic function groups. They performed supine ergometer exercise and blood samples were drawn at rest and at peak exercise. After dynamic exercise, plasma norepinephrine was significantly (p < 0.05) increased in patients with preserved LV function, whereas it was not altered in patients with impaired LV function (norepinephrine 20.8 +/- 20.5 vs 45.8 +/- 41.9, respectively). We observed no differences in basal or peak levels of neurohormonal factors, including plasma renin activity, aldosterone, and brain natriuretic peptide (BNP), between the groups. Although the plasma levels of angiotensin I and II were not different in the two groups at rest or at peak exercise, their increasing ratios from rest to peak exercise were significantly higher in patients with impaired LV function compared to those with preserved LV function (angiotensin I; -18.6 +/- 31.0% vs 64.8 +/- 66.5%, p < 0.05, angiotensin II; -5.9 +/- 41.2% vs 60.7 +/- 40.4% , p < 0.05). These results suggest that the increasing ratios of angiotensin I and II are superior to BNP as predictors of LV dysfunction, and that the sympathetic nervous system has already been activated even at rest and did not respond to dynamic exercise in patients with LV dysfunction in ischemic heart disease.
authors.affiliation: Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sekiguchi
authors.forename: T
authors.initials: T
authors.lastname: Kanda
authors.forename: Z
authors.initials: Z
authors.lastname: Ono
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Yokoyama
authors.forename: Y
authors.initials: Y
authors.lastname: Aihara
authors.forename: T
authors.initials: T
authors.lastname: Toyama
authors.forename: T
authors.initials: T
authors.lastname: Sakamaki
authors.forename: I
authors.initials: I
authors.lastname: Kobayashi
authors.forename: M
authors.initials: M
authors.lastname: Kurabayashi
authors.forename: R
authors.initials: R
authors.lastname: Nagai
mesh_terms: D000368:Aged; D000803:Angiotensin I / Q000097:blood*; D000804:Angiotensin II / Q000097:blood*; D005080:Exercise Test; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000503:physiopathology*; D010865:Pilot Projects; D012084:Renin-Angiotensin System / Q000502:physiology; D013318:Stroke Volume; D013564:Sympathetic Nervous System / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis*; D016277:Ventricular Function, Left
chemical_list: D000804:Angiotensin II; D000803:Angiotensin I