PMID- 1969707
OWN - NLM
STAT- MEDLINE
DCOM- 19900504
LR  - 20190626
IS  - 0002-8703 (Print)
IS  - 0002-8703 (Linking)
VI  - 119
IP  - 4
DP  - 1990 Apr
TI  - Evidence against spare or uncoupled beta-adrenoceptors in the human heart.
PG  - 899-904
AB  - It is well established that increasing degrees of heart failure are accompanied 
      by a reduced density of myocardial beta-adrenoceptors. It is unclear, however, 
      whether all beta-adrenoceptors in the cardiac cell membrane are coupled to the 
      effector system or whether "spare receptors" or "uncoupled" beta-adrenoceptors 
      also exist. To investigate this, we measured the density of beta-adrenoceptors 
      and the positive inotropic response to isoprenaline in preparations from the same 
      human hearts. The myocardium from nonfailing hearts had significantly (p less 
      than 0.01) higher numbers of beta-adrenoceptors (104 +/- 7 fmol/mg protein) 
      compared with tissue from moderately (mitral valve disease, New York Heart 
      Association [NYHA] class II to III, 60 +/- 2.8 fmol/mg protein) and terminally 
      (dilated cardiomyopathy, NYHA class IV, 35 +/- 2.7 fmol/mg protein) failing human 
      hearts. The KD values of the drug-receptor complexes did not differ within the 
      different patient groups. There was a linear relationship (r = 0.97) between the 
      beta-adrenoceptor density measured and the maximally obtainable positive 
      inotropic effect elicited by isoprenaline in the three groups tested. Thus there 
      seem to be no spare beta-adrenoceptors, that is, receptors not required for the 
      production of the maximal inotropic response in the left ventricular human 
      myocardium, and there are no uncoupled beta-adrenoceptors. The beta-adrenoceptors 
      associated with the plasma membrane (marker: 3H-ouabain binding sites) remained 
      functionally active. In addition, these results indicate that either there is no 
      amplifier system behind the receptor level or it remains unchanged in the failing 
      left ventricular human myocardium under the conditions tested.
FAU - Schwinger, R H
AU  - Schwinger RH
AD  - Medizinische Klinik I, Universitat Munchen, FRG.
FAU - Bohm, M
AU  - Bohm M
FAU - Erdmann, E
AU  - Erdmann E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 0 (Propanolamines)
RN  - 0 (Receptors, Adrenergic, beta)
RN  - L628TT009W (Isoproterenol)
RN  - R89UMZ82MJ (CGP 12177)
SB  - IM
MH  - Adrenergic beta-Antagonists
MH  - Adult
MH  - Binding Sites
MH  - Cell Membrane/analysis
MH  - Electric Stimulation
MH  - Female
MH  - Heart/*innervation
MH  - Humans
MH  - Isoproterenol/pharmacology
MH  - Male
MH  - Myocardial Contraction/drug effects
MH  - Myocardium/analysis
MH  - Papillary Muscles/analysis/physiology
MH  - Propanolamines
MH  - Radioligand Assay
MH  - Receptors, Adrenergic, beta/*analysis
EDAT- 1990/04/01 00:00
MHDA- 1990/04/01 00:01
CRDT- 1990/04/01 00:00
PHST- 1990/04/01 00:00 [pubmed]
PHST- 1990/04/01 00:01 [medline]
PHST- 1990/04/01 00:00 [entrez]
AID - S0002-8703(05)80329-1 [pii]
AID - 10.1016/s0002-8703(05)80329-1 [doi]
PST - ppublish
SO  - Am Heart J. 1990 Apr;119(4):899-904. doi: 10.1016/s0002-8703(05)80329-1.