title: Angiotensin II in the evolution of experimental heart failure.
abstract: Although angiotensin II (Ang II) has been implicated in the pathophysiology of congestive heart failure, its temporal and regional changes during the development and progression of the disease are poorly defined. Our objective was to assess circulating, renal, cardiac, and vascular Ang II in a canine model of rapid ventricular pacing-induced heart failure that evolves from early left ventricular dysfunction to overt congestive heart failure. Ang II was measured by radioimmunoassay with low cross-reactivity to other angiotensins. Control, early left ventricular dysfunction, and overt congestive heart failure dogs were studied. Early left ventricular dysfunction was characterized by impaired cardiac function, cardiac enlargement, preserved renal perfusion pressure, maintained urinary sodium excretion, and normal plasma renin activity. Overt congestive heart failure was characterized by further impaired cardiac function and cardiac enlargement, reduced renal perfusion pressure, urinary sodium retention, and increased plasma renin activity and plasma Ang II. In early left ventricular dysfunction dogs, renal cortical, renal medullary, ventricular, and aortic Ang II were unchanged, and atrial Ang II was decreased. In overt congestive heart failure dogs, Ang II was increased in the kidney and heart compared with normal dogs and in all tissues compared with early left ventricular dysfunction dogs. The greatest increase in tissue Ang II occurred in the renal medulla. We conclude that early increases in local renal, myocardial, and vascular Ang II do not occur in this model of early left ventricular dysfunction and may even be suppressed. In contrast, increased myocardial and particularly renal Ang II in association with increased circulating Ang II are hallmarks of overt experimental congestive heart failure. These studies provide new insights into the temporal and regional alterations in Ang II during the progression of experimental congestive heart failure.
authors.affiliation: Cardiorenal Research Laboratory, Mayo Clinic and Foundation, Rochester, Minn. 55905, USA. luchner.andreas@mayo.edu
authors.forename: A
authors.initials: A
authors.lastname: Luchner
authors.forename: T L
authors.initials: TL
authors.lastname: Stevens
authors.forename: D D
authors.initials: DD
authors.lastname: Borgeson
authors.forename: M M
authors.initials: MM
authors.lastname: Redfield
authors.forename: J E
authors.initials: JE
authors.lastname: Bailey
authors.forename: S M
authors.initials: SM
authors.lastname: Sandberg
authors.forename: D M
authors.initials: DM
authors.lastname: Heublein
authors.forename: J C
authors.initials: JC
authors.lastname: Burnett
mesh_terms: D000804:Angiotensin II / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D001011:Aorta / Q000378:metabolism; D004285:Dogs; D006333:Heart Failure / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D006728:Hormones / Q000097:blood; D007668:Kidney / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009318:Natriuresis; D016277:Ventricular Function, Left
chemical_list: D006728:Hormones; D000804:Angiotensin II