PMID- 2557323
OWN - NLM
STAT- MEDLINE
DCOM- 19900208
LR  - 20171213
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 67
IP  - 5
DP  - 1989 Nov
TI  - Skeletal muscle beta-receptors and isoproterenol-stimulated vasodilation in 
      canine heart failure.
PG  - 2026-31
AB  - To investigate whether heart failure alters beta-adrenergic receptors on skeletal 
      muscle and its associated vasculature, the density of beta-adrenergic receptors, 
      isoproterenol-stimulated adenylate cyclase activity, and coupling of the guanine 
      nucleotide-binding regulatory protein were compared in 18 control dogs and 16 
      dogs with heart failure induced by 5-8 wk of ventricular pacing at 260 beats/min. 
      Hindlimb vascular responses to isoproterenol were compared in eight controls and 
      eight of the dogs with heart failure. In dogs with heart failure, the density of 
      beta-receptors on skeletal muscle was reduced in both gastrocnemius (control: 50 
      +/- 5; heart failure: 33 +/- 8 fmol/mg of protein) and semitendinosus muscle 
      (control: 43 +/- 9; heart failure: 27 +/- 9 fmol/mg of protein, both P less than 
      0.05). Receptor coupling to the ternary complex, as determined by isoproterenol 
      competition curves with and without guanosine 5'-triphosphate (GTP), was 
      unchanged. Isoproterenol-stimulated adenylate cyclase activity was significantly 
      decreased in semitendinosus muscle (control: 52.4 +/- 4.6; heart failure: 36.5 
      +/- 9.5 pmol.mg-1.min-1; P less than 0.05) and tended to be decreased in 
      gastrocnemius muscle (control: 40.1 +/- 8.5; heart failure: 33.5 +/- 4.5 
      pmol.mg-1.min-1; P = NS). Isoproterenol-induced hindlimb vasodilation was not 
      significantly different in controls and in dogs with heart failure. These 
      findings suggest that heart failure causes downregulation of skeletal muscle 
      beta-adrenergic receptors, probably due to receptor exposure to elevated 
      catecholamine levels, but does not reduce beta-receptor-mediated vasodilation in 
      muscle.
FAU - Frey, M J
AU  - Frey MJ
AD  - Department of Medicine and Pharmacology, University of Pennsylvania, Philadelphia 
      19104.
FAU - Lanoce, V
AU  - Lanoce V
FAU - Molinoff, P B
AU  - Molinoff PB
FAU - Wilson, J R
AU  - Wilson JR
LA  - eng
GR  - HL-01766/HL/NHLBI NIH HHS/United States
GR  - NS-18479/NS/NINDS NIH HHS/United States
GR  - R0-1 HL-34834/HL/NHLBI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (Receptors, Adrenergic, beta)
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - EC 4.6.1.1 (Adenylyl Cyclases)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - Adenylyl Cyclases/metabolism
MH  - Animals
MH  - Binding, Competitive
MH  - Cardiac Output, Low/*metabolism
MH  - Data Interpretation, Statistical
MH  - Dogs
MH  - Guanosine Triphosphate/metabolism
MH  - Hemodynamics
MH  - Hindlimb
MH  - Iodine Radioisotopes
MH  - Isoproterenol/*pharmacology
MH  - Muscles/blood supply/drug effects/*metabolism
MH  - Receptors, Adrenergic, beta/*metabolism
MH  - Vasodilation/*drug effects
EDAT- 1989/11/01 00:00
MHDA- 1989/11/01 00:01
CRDT- 1989/11/01 00:00
PHST- 1989/11/01 00:00 [pubmed]
PHST- 1989/11/01 00:01 [medline]
PHST- 1989/11/01 00:00 [entrez]
AID - 10.1152/jappl.1989.67.5.2026 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 1989 Nov;67(5):2026-31. doi: 10.1152/jappl.1989.67.5.2026.