PMID- 10644586
OWN - NLM
STAT- MEDLINE
DCOM- 20000607
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 278
IP  - 1
DP  - 2000 Jan
TI  - Adenosine is not responsible for local metabolic control of coronary blood flow 
      in dogs during exercise.
PG  - H74-84
AB  - The purpose of this investigation was to quantitatively evaluate the role of 
      adenosine in coronary exercise hyperemia. Dogs (n = 10) were chronically 
      instrumented with catheters in the aorta and coronary sinus, and a flow probe on 
      the circumflex coronary artery. Cardiac interstitial adenosine concentration was 
      estimated from arterial and coronary venous plasma concentrations using a 
      previously tested mathematical model. Coronary blood flow, myocardial oxygen 
      consumption, heart rate, and aortic pressure were measured at rest and during 
      graded treadmill exercise with and without adenosine receptor blockade with 
      either 8-phenyltheophylline (8-PT) or 8-p-sulfophenyltheophylline (8-PST). In 
      control vehicle dogs, exercise increased myocardial oxygen consumption 4.2-fold, 
      coronary blood flow 3.8-fold, and heart rate 2.5-fold, whereas mean aortic 
      pressure was unchanged. Coronary venous plasma adenosine concentration was little 
      changed with exercise, and the estimated interstitial adenosine concentration 
      remained well below the threshold for coronary vasodilation. Adenosine receptor 
      blockade did not significantly alter myocardial oxygen consumption or coronary 
      blood flow at rest or during exercise. Coronary venous and estimated interstitial 
      adenosine concentration did not increase to overcome the receptor blockade with 
      either 8-PT or 8-PST as would be predicted if adenosine were part of a high-gain, 
      negative-feedback, local metabolic control mechanism. These results demonstrate 
      that adenosine is not responsible for local metabolic control of coronary blood 
      flow in dogs during exercise.
FAU - Tune, J D
AU  - Tune JD
AD  - Department of Physiology and Biophysics, University of Washington School of 
      Medicine, Seattle, Washington 98195, USA.
FAU - Richmond, K N
AU  - Richmond KN
FAU - Gorman, M W
AU  - Gorman MW
FAU - Olsson, R A
AU  - Olsson RA
FAU - Feigl, E O
AU  - Feigl EO
LA  - eng
GR  - HL-07403/HL/NHLBI NIH HHS/United States
GR  - HL-49822/HL/NHLBI NIH HHS/United States
GR  - RR-01243/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Purinergic P1 Receptor Antagonists)
RN  - 0 (Pyridines)
RN  - 0 (Receptors, Endothelin)
RN  - 0 (Tetrazoles)
RN  - 64J9J55263 (tezosentan)
RN  - 80206-91-3 (8-(4-sulfophenyl)theophylline)
RN  - C137DTR5RG (Theophylline)
RN  - E6M543P3BL (8-phenyltheophylline)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenosine/*physiology
MH  - Animals
MH  - Coronary Circulation/*physiology
MH  - Dogs
MH  - Dose-Response Relationship, Drug
MH  - Male
MH  - Motor Activity/*physiology
MH  - Purinergic P1 Receptor Antagonists
MH  - Pyridines/pharmacology
MH  - Receptors, Endothelin/physiology
MH  - Tetrazoles/pharmacology
MH  - Theophylline/analogs & derivatives/pharmacology
EDAT- 2000/01/25 09:00
MHDA- 2000/06/10 09:00
CRDT- 2000/01/25 09:00
PHST- 2000/01/25 09:00 [pubmed]
PHST- 2000/06/10 09:00 [medline]
PHST- 2000/01/25 09:00 [entrez]
AID - 10.1152/ajpheart.2000.278.1.H74 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2000 Jan;278(1):H74-84. doi: 
      10.1152/ajpheart.2000.278.1.H74.