scholarly journals Unveiling the Mechanism of Coronary Metabolic Vasodilation

2015 ◽  
Vol 117 (7) ◽  
pp. 589-591 ◽  
Author(s):  
Dawid Chabowski ◽  
David Gutterman
Keyword(s):  
Metabolic Vasodilation

Endogenous adenosine modulates alpha 2- but not alpha 1-adrenergic constriction of coronary arterioles

1995 ◽  
Vol 268 (6) ◽  
pp. H2487-H2494 ◽  
Author(s):  
D. V. DeFily ◽  
J. L. Patterson ◽  
W. M. Chilian
Keyword(s):  
Coronary Circulation ◽  
Beta Blockade ◽  
Adenosine Receptor Antagonist ◽  
Endogenous Production ◽  
Adenosine Antagonism ◽  
Metabolic Stimulation ◽  
Metabolic Vasodilation ◽  
Baseline Diameter ◽  
Made In ◽  
Coronary Arterioles

In the coronary circulation alpha-adrenergic constriction competes with metabolic vasodilation. Because adenosine is produced by the working myocardium and metabolic stimulation results in arteriolar dilation, we tested the hypothesis that coronary arteriolar alpha-adrenergic constriction is attenuated by the endogenous production of adenosine. To test this hypothesis, using fluorescence microscopy during stroboscopic epi-illumination of the epicardial microvasculature, we measured the diameter of coronary arterioles in anesthetized open-chest dogs. Measurements were made in the presence of beta-blockade during selective alpha 1- or alpha 2-adrenoceptor activation (phenylephrine or B-HT-933, respectively) before and in the presence of the nonselective adenosine receptor antagonist 8-p-sulfophenyltheophylline (8-pSPT) and expressed as a percent change in microvascular diameter relative to baseline. alpha 1-Activation produced constriction of coronary arterioles under control conditions, which was not augmented after adenosine antagonism (-12 +/- 2 vs. -7 +/- 3%). In contrast, alpha 2-activation did not constrict coronary arterioles under control conditions; however, blockade of adenosine receptors unmasked a significant constriction (0 +/- 2 vs. -7 +/- 2%, P < 0.05). Also adenosine antagonism did not significantly alter the baseline diameter of coronary arterioles. These results demonstrate that endogenously produced adenosine modulates alpha 2-adrenergic constriction of coronary arterioles but not alpha 1-adrenergic constriction, and therefore we speculate that the competition between alpha-adrenergic constriction and metabolic vasodilation is mediated by the alpha 1-adrenoceptor.

Nitrite-derived nitric oxide: a possible mediator of 'acidic-metabolic' vasodilation

2001 ◽  
Vol 171 (1) ◽  
pp. 9-16 ◽  
Author(s):  
A. Modin ◽  
H. Bjorne ◽  
M. Herulf ◽  
K. Alving ◽  
E. Weitzberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Vasodilation

Role of pertussis toxin-sensitive G protein in metabolic vasodilation of coronary microcirculation

2000 ◽  
Vol 279 (4) ◽  
pp. H1819-H1829 ◽  
Author(s):  
Toshinori Tanikawa ◽  
Hiroshi Kanatsuka ◽  
Ryohji Koshida ◽  
Mitsuaki Tanaka ◽  
Akihiko Sugimura ◽  
...  
Keyword(s):  
G Protein ◽  
Pertussis Toxin ◽  
Atrial Pacing ◽  
Metabolic Demand ◽  
Before And After ◽  
Vehicle Treatment ◽  
Rapid Pacing ◽  
Metabolic Stimulation ◽  
Metabolic Vasodilation

We have previously demonstrated that pertussis toxin (PTX)-sensitive G protein (GPTX) plays a major role in coronary microvascular vasomotion during hypoperfusion. We aimed to elucidate the role of GPTX during increasing metabolic demand. In 18 mongrel dogs, coronary arteriolar diameters were measured by fluorescence microangiography using a floating objective. Myocardial oxygen consumption (MV˙o 2) was increased by rapid left atrial pacing. In six dogs, PTX (300 ng/ml) was superfused onto the heart surface for 2 h to locally block GPTX. In eight dogs, the vehicle (Krebs solution) was superfused in the same way. Before and after each treatment, the diameters were measured during control (130 beats/min) and rapid pacing (260 beats/min) in each group. Metabolic stimulation before and after the vehicle treatment caused 8.6 ± 1.8 and 16.1 ± 3.6% dilation of coronary arterioles <100 μm in diameter (57 ± 8 μm at control, n = 10), respectively. PTX treatment clearly abolished the dilation of arterioles (12.8 ± 2.5% before and 0.9 ± 1.6% after the treatment, P < 0.001 vs. vehicle; 66 ± 8 μm at control, n = 11) in response to metabolic stimulation. The increases in MV˙o 2 and coronary flow velocity were comparable between the vehicle and PTX groups. In four dogs, 8-phenyltheophylline (10 μM, superfusion for 30 min) did not affect the metabolic dilation of arterioles (15.3 ± 2.0% before and 16.4 ± 3.8% after treatment; 84.3 ± 11.0 μm at control, n = 8). Thus we conclude that GPTXplays a major role in regulating the coronary microvascular tone during active hyperemia, and adenosine does not contribute to metabolic vasodilation via GPTX activation.

The effect of ATP-sensitive potassium (KATP) channel inhibition on metabolic vasodilation in human skeletal muscle vasculature

2000 ◽  
Vol 9 (3) ◽  
pp. A110
Author(s):  
H.M.O. Farouque ◽  
R.A.P. Skyrme-Jones ◽  
M.J. Zhang ◽  
R.C. O'Brien ◽  
I.T. Meredith
Keyword(s):  
Skeletal Muscle ◽  
Katp Channel ◽  
Human Skeletal Muscle ◽  
Channel Inhibition ◽  
Metabolic Vasodilation

Nitrite-derived nitric oxide: a possible mediator of ‘acidic-metabolic’ vasodilation

2001 ◽  
Vol 171 (1) ◽  
pp. 9-16 ◽  
Author(s):  
A. Modin ◽  
H. Björne ◽  
M. Herulf ◽  
K. Alving ◽  
E. Weitzberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Vasodilation

Adenosine's role in coronary vasodilation induced by atrial pacing and norepinephrine

1982 ◽  
Vol 243 (4) ◽  
pp. H536-H545 ◽  
Author(s):  
J. P. Manfredi ◽  
H. V. Sparks
Keyword(s):  
Left Atrial ◽  
Myocardial Oxygen Consumption ◽  
Atrial Pacing ◽  
Coronary Vasodilation ◽  
Vascular Conductance ◽  
Norepinephrine Infusion ◽  
Anesthetized Dogs ◽  
The Difference ◽  
Arterial Plasma ◽  
Metabolic Vasodilation

If adenosine (ADO) mediates metabolic vasodilation in the heart, increases in interstitial ADO (ISF[ADO]) must accompany increases in coronary vascular conductance. We tested this using ADO release, defined as the difference in [ADO] in coronary venous and arterial plasma multiplied by coronary plasma flow, as an index of ISF[ADO]. Pentobarbital-anesthetized dogs received intravenous norepinephrine or left atrial pacing, and the resulting changes in coronary blood flow (delta CBF), conductance (delta C), myocardial oxygen consumption (delta VO2), and ADO release (delta RADO) were measured. If ISF[ADO] and C are coupled, the ratio delta RADO/delta C should be greater than zero. For dogs receiving atrial pacing, the ratios delta RADO/delta C, delta RADO/delta CBF, and delta RADO/delta VO2 equal -2.4 +/- 2.2 nmol . mmHg-1 . ml-1, -0.022 +/- 0.020 nmol/ml, and -0.13 +/- 0.12 nmol/ml, respectively. These values do not differ from zero. For dogs receiving norepinephrine, delta RADO/delta C, delta RADO/delta CBF, and delta RADO/delta VO2 equal 9.7 +/- 1.8, 0.051 +/- 0.017, and 0.44 +/- 0.13, respectively. These values are greater than zero (P less than 0.05). These differences between atrial pacing and norepinephrine infusion rate observed despite similar changes in C, CBF, and VO2. We conclude that ADO may mediate the vasodilation induced by norepinephrine, but not atrial pacing.

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