Angiotensin II in the evolution of experimental heart failure

Andreas Luchner, Tracy L. Stevens, Daniel Dean Borgeson, Margaret May Redfield, Jane E. Bailey, Sharon M. Sandberg, Denise M. Heublein, John C Jr. Burnett

Research output: Contribution to journalArticle

59 Citations (Scopus)

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 progressive of experimental congestive heart failure.

Original languageEnglish (US)
Pages (from-to)472-477
Number of pages6
JournalHypertension
Volume28
Issue number3
StatePublished - Sep 1996

Fingerprint

Angiotensin II
Heart Failure
Left Ventricular Dysfunction
Kidney
Dogs
Renin
Blood Vessels
Perfusion
Sodium
Pressure
Urinary Retention
Angiotensins
Radioimmunoassay
Disease Progression
Canidae

Keywords

  • aorta
  • heart
  • heart failure
  • kidney
  • natriuretic peptide

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Luchner, A., Stevens, T. L., Borgeson, D. D., Redfield, M. M., Bailey, J. E., Sandberg, S. M., ... Burnett, J. C. J. (1996). Angiotensin II in the evolution of experimental heart failure. Hypertension, 28(3), 472-477.

Angiotensin II in the evolution of experimental heart failure. / Luchner, Andreas; Stevens, Tracy L.; Borgeson, Daniel Dean; Redfield, Margaret May; Bailey, Jane E.; Sandberg, Sharon M.; Heublein, Denise M.; Burnett, John C Jr.

In: Hypertension, Vol. 28, No. 3, 09.1996, p. 472-477.

Research output: Contribution to journalArticle

Luchner, A, Stevens, TL, Borgeson, DD, Redfield, MM, Bailey, JE, Sandberg, SM, Heublein, DM & Burnett, JCJ 1996, 'Angiotensin II in the evolution of experimental heart failure', Hypertension, vol. 28, no. 3, pp. 472-477.
Luchner A, Stevens TL, Borgeson DD, Redfield MM, Bailey JE, Sandberg SM et al. Angiotensin II in the evolution of experimental heart failure. Hypertension. 1996 Sep;28(3):472-477.
Luchner, Andreas ; Stevens, Tracy L. ; Borgeson, Daniel Dean ; Redfield, Margaret May ; Bailey, Jane E. ; Sandberg, Sharon M. ; Heublein, Denise M. ; Burnett, John C Jr. / Angiotensin II in the evolution of experimental heart failure. In: Hypertension. 1996 ; Vol. 28, No. 3. pp. 472-477.
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