PMID- 10519161
OWN - NLM
STAT- MEDLINE
DCOM- 19991124
LR  - 20191103
IS  - 1081-650X (Print)
IS  - 1081-650X (Linking)
VI  - 111
IP  - 5
DP  - 1999 Sep-Oct
TI  - The natriuretic peptides in heart failure: diagnostic and therapeutic potentials.
PG  - 406-16
AB  - The natriuretic peptides are a group of structurally similar but genetically 
      distinct peptides that have diverse actions in cardiovascular, renal, and 
      endocrine homeostasis. Atrial natriuretic peptide (ANP) and brain natriuretic 
      peptide (BNP) are of myocardial cell origin and C-type natriuretic peptide (CNP) 
      is of endothelial origin. ANP and BNP bind to the natriuretic peptide-A receptor 
      (NPR-A), which, via 3',5'-cyclic guanosine monophosphate (cGMP), mediates 
      natriuresis, vasodilation, renin inhibition, antimitogenesis, and lusitropic 
      properties. CNP lacks natriuretic actions but possesses vasodilating and 
      growth-inhibiting actions via the guanylyl cyclase-linked natriuretic peptide-B 
      receptor (NPR-B). All three peptides are cleared by the natriuretic peptide-C 
      receptor (NPR-C) and are degraded by the ectoenzyme neutral endopeptidase 24.11 
      (NEP), both of which are widely expressed in the kidneys, lungs, and the vascular 
      wall. Congestive heart failure (CHF) represents a pathological state in which the 
      activation of the natriuretic peptides exceeds those of all other states. In this 
      brief review, we will attempt to provide an update on important issues regarding 
      natriuretic peptides in CHF, with a focus on their functional importance as a 
      beneficial humoral response in asymptomatic left ventricular dysfunction (LVD), 
      the mechanisms of natriuretic peptide hyporesponsiveness in severe heart failure, 
      the diagnostic and prognostic significance of the natriuretic peptides in CHF, 
      and the therapeutic potential of the natriuretic peptides in this multiorgan 
      syndrome.
FAU - Chen, H H
AU  - Chen HH
AD  - Cardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic 
      and Foundation, Rochester, MN 55905, USA.
FAU - Burnett, J C Jr
AU  - Burnett JC Jr
LA  - eng
GR  - HL 07111/HL/NHLBI NIH HHS/United States
GR  - HL 36634/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Proc Assoc Am Physicians
JT  - Proceedings of the Association of American Physicians
JID - 9514310
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Enzyme Inhibitors)
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
RN  - 127869-51-6 (Natriuretic Peptide, C-Type)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
RN  - EC 3.4.24.11 (Neprilysin)
SB  - IM
MH  - Amino Acid Sequence
MH  - Angiotensin-Converting Enzyme Inhibitors/therapeutic use
MH  - Animals
MH  - Atrial Natriuretic Factor/genetics/*metabolism
MH  - Enzyme Inhibitors/therapeutic use
MH  - Heart Failure/*diagnosis/*drug therapy/metabolism
MH  - Humans
MH  - Molecular Sequence Data
MH  - Natriuretic Peptide, Brain/genetics/*metabolism/therapeutic use
MH  - Natriuretic Peptide, C-Type/genetics/*metabolism
MH  - Neprilysin/antagonists & inhibitors/metabolism
MH  - Prognosis
MH  - Ventricular Dysfunction, Left/metabolism
RF  - 73
EDAT- 1999/10/16 09:00
MHDA- 2001/03/28 10:01
CRDT- 1999/10/16 09:00
PHST- 1999/10/16 09:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1999/10/16 09:00 [entrez]
AID - 10.1111/paa.1999.111.5.406 [doi]
PST - ppublish
SO  - Proc Assoc Am Physicians. 1999 Sep-Oct;111(5):406-16. doi: 
      10.1111/paa.1999.111.5.406.