PMID- 2464110
OWN - NLM
STAT- MEDLINE
DCOM- 19890303
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 12
IP  - 3
DP  - 1988 Sep
TI  - Alpha-adrenoceptors and alpha-adrenoceptor-mediated positive inotropic effects in 
      failing human myocardium.
PG  - 357-64
AB  - Experiments were designed to characterize cardiac alpha-adrenoceptors and the 
      alpha-adrenoceptor-mediated positive inotropic effects in human myocardial tissue 
      from patients with moderate New York Heart Association (NYHA) class II-III and 
      severe (NYHA class IV) heart failure. The number of cardiac alpha-adrenoceptors 
      was low but similar in moderate and severe heart failure (NYHA class II-III: 6.7 
      +/- 0.8 fmol/mg protein 3H-prazosin bound, n = 12; NYHA class IV: 7.4 +/- 0.9 
      fmol/mg protein 3H-prazosin bound, n = 9; NS). Correspondingly, the 
      alpha-adrenoceptor-mediated positive inotropic effect (phenylephrine in the 
      presence of propranolol) did not significantly differ in both groups. In the same 
      hearts, the number of beta-adrenoceptors was measured. The number of 
      beta-adrenoceptors was significantly reduced in severe heart failure (NYHA class 
      II-III: 22.0 +/- 1.5 fmol/mg protein 3H-CGP 12177 bound, n = 12; NYHA class IV: 
      11.9 +/- 0.8 fmol/mg protein 3H-CGP 12177 bound, n = 9; p less than 0.05). The 
      positive inotropic effect of isoprenaline was significantly reduced in NYHA class 
      IV. The positive inotropic effect of Ca2+ was similar in both groups. In 
      conclusion, cardiac beta-adrenoceptors and the beta-adrenoceptor-mediated 
      positive inotropic effects were reduced in severely failing myocardium. Cardiac 
      alpha-adrenoceptors and the positive inotropic effect resulting from their 
      stimulation is unchanged. Therefore, down regulation in response to increased 
      sympathetic stimulation or a compensatory increase of alpha-adrenoceptors does 
      obviously not occur in the human heart.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Bohm, M
AU  - Bohm M
AD  - Medizinische Klinik I der Universitat Munchen, Klinikum Grosshadern, Munich, 
      F.R.G.
FAU - Diet, F
AU  - Diet F
FAU - Feiler, G
AU  - Feiler G
FAU - Kemkes, B
AU  - Kemkes B
FAU - Erdmann, E
AU  - Erdmann E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Receptors, Adrenergic, alpha)
RN  - 0 (Receptors, Adrenergic, beta)
RN  - 1WS297W6MV (Phenylephrine)
RN  - L628TT009W (Isoproterenol)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Calcium/pharmacology
MH  - Female
MH  - Heart Failure/*physiopathology
MH  - Humans
MH  - In Vitro Techniques
MH  - Isoproterenol/pharmacology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Contraction/*drug effects
MH  - Papillary Muscles/metabolism
MH  - Phenylephrine/pharmacology
MH  - Receptors, Adrenergic, alpha/*physiopathology
MH  - Receptors, Adrenergic, beta/drug effects/metabolism
EDAT- 1988/09/01 00:00
MHDA- 1988/09/01 00:01
CRDT- 1988/09/01 00:00
PHST- 1988/09/01 00:00 [pubmed]
PHST- 1988/09/01 00:01 [medline]
PHST- 1988/09/01 00:00 [entrez]
AID - 10.1097/00005344-198809000-00015 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1988 Sep;12(3):357-64. doi: 
      10.1097/00005344-198809000-00015.