Subcutaneous BNP administration in experimental mild heart failure: A novel therapeutic strategy

Hh, Chen; Grantham, J.Aaron; Schirger, JA; Jougasaki, Michihisa; Lisý, Ondřej; Redfield, MM; Burnett, J. C.

doi:10.1016/s1071-9164(98)90069-0

Cited by 1 publication

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“…[31][32][33][34] Chen and colleagues previously reported that 10-day subcutaneous BNP in experimental HF had beneficial effects to unload the heart without evidence of tolerance. 35,36 We extended this concept of chronic subcutaneous BNP to human studies and reported the first demonstration that a 3-day period of subcutaneous BNP increases circulating concentrations of BNP, activates plasma and urinary cGMP, and, more importantly, enhances sodium excretion and reduces activation of the RAAS. 37 More recently, we demonstrated that the antialdosterone properties of BNP are maintained in a model of overt HF even in the presence of a loop diuretic.…”

Section: Sodium-and Aldosterone-regulating Actionsmentioning

confidence: 99%

Natriuretic Peptides: Novel Therapeutic Targets in Heart Failure

Cataliotti

Burnett

2005

Journal of Investigative Medicine

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Since the discovery of the cardiac hormone atrial natriuretic peptide by de Bold and colleagues in 1981, the field of natriuretic peptides has significantly advanced with translation of new knowledge to the clinical practice of heart failure. This new knowledge builds on the importance of cardiorenal mechanisms that contribute to optimal cardiovascular regulation. Recent investigations by our group and others have also established the direct myocardial actions of the natriuretic peptides, broadening their therapeutic potential beyond renal mechanisms. Indeed, a potential therapeutic target is cardiac remodeling and fibrosis based on the unique cardiorenal and humoral protective properties that natriuretic peptides possess. We review new insights into the natriuretic peptide system and specifically focus on the possible role of natriuretic peptides as a new therapeutic strategy to limit cardiac remodeling and fibrosis to delay worsening of cardiac function and the progression of heart failure.

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