Adenosine receptor blockade and fetal breathing during hypoxia in sheep

1998 ◽  
Vol 5 (1) ◽  
pp. 160A-160A
Author(s):  
A CHAU ◽  
B KOOS
Keyword(s):  
Adenosine Receptor ◽  
Receptor Blockade ◽  
Fetal Breathing

scholarly journals EFFECT OF ADENOSINE RECEPTOR BLOCKADE ON HYPOGLYCEMIA-INDUCED DILATIONS OF PIAL ARTERIOLES (PA) IN PIGLETS

1992 ◽  
Vol 32 (5) ◽  
pp. 631-631
Author(s):  
Vineta J Ruth ◽  
Jeffrey M Gidday ◽  
Ernesto R Gonzales ◽  
T S Park
Keyword(s):  
Adenosine Receptor ◽  
Receptor Blockade ◽  
Pial Arterioles

scholarly journals Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

2011 ◽  
Vol 110 (5) ◽  
pp. 1181-1189 ◽  
Author(s):  
Darren P. Casey ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Steady State ◽  
Arterial Pressure ◽  
Brachial Artery ◽  
Adenosine Receptor ◽  
Receptor Blockade ◽  
Independent Manner ◽  
Control Value ◽  
Percent Recovery

We previously demonstrated that nitric oxide (NO) contributes to compensatory vasodilation in the contracting human forearm subjected to acute hypoperfusion. We examined the potential role of an adenosine-NO interaction to this response in 17 male subjects (25 ± 2 yr). In separate protocols subjects performed rhythmic forearm exercise (20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included exercise before inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and local [brachial artery catheter pressure (BAP)] and systemic [mean arterial pressure (MAP); Finometer] arterial pressure were measured. In protocol 1 ( n = 10), exercise was repeated during nitric oxide synthase inhibition [ NG-monomethyl-l-arginine (l-NMMA)] alone and during l-NMMA-aminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-l-NMMA. Forearm vascular conductance (FVC; ml·min−1·100 mmHg−1) was calculated from blood flow (ml/min) and BAP (mmHg). Percent recovery in FVC during inflation was calculated as (steady-state inflation + exercise value − nadir)/[steady-state exercise (control) value − nadir]. In protocol 1, percent recovery in FVC was 108 ± 8% during the control (no drug) trial. Percent recovery in FVC was attenuated with inhibition of NO formation alone (78 ± 9%; P < 0.01 vs. control) and was attenuated further with combined inhibition of NO and adenosine (58 ± 9%; P < 0.01 vs. l-NMMA). In protocol 2, percent recovery was reduced with adenosine receptor blockade (74 ± 11% vs. 113 ± 6%, P < 0.01) compared with control drug trials. Percent recovery in FVC was attenuated further with combined inhibition of adenosine and NO (48 ± 11%; P < 0.05 vs. aminophylline). Our data indicate that adenosine contributes to compensatory vasodilation in an NO-independent manner during exercise with acute hypoperfusion.

Effect of adenosine receptor blockade: preventing protective preconditioning depends on time of initiation

1993 ◽  
Vol 265 (2) ◽  
pp. H504-H508 ◽  
Author(s):  
J. D. Thornton ◽  
C. S. Thornton ◽  
J. M. Downey
Keyword(s):  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Adenosine Receptor ◽  
Adenosine Receptors ◽  
Receptor Blockade ◽  
Risk Zone ◽  
Time Points ◽  
Adenosine Receptor Antagonist ◽  
Rabbit Myocardium ◽  
Ischemic Period

Ischemic preconditioning protects the rabbit myocardium from infarction from a subsequent ischemia, and adenosine receptors appear to be involved in this protection. The present study attempts to determine when adenosine receptors must be occupied to achieve protection by infusing the adenosine receptor antagonist PD-115,199 at various time points during the study. Open-chest rabbits were subjected to 30 min of regional ischemia followed by 3 h of reperfusion and had 38 +/- 4% infarction of the risk zone. When hearts were preconditioned by 5 min of ischemia and 10 min reperfusion before the 30-min period of ischemia, only 9 +/- 2% infarction occurred. PD-115,199 given 5 min before the ischemic preconditioning episode blocked the protective effect of preconditioning (39 +/- 5% infarction). PD-115,199 also blocked the protection when given between the ischemic preconditioning episode and the 30-min period of ischemia (30 +/- 4% infarction). PD-115,199 given at the end of 30 min of ischemia did not block protection in preconditioned (PC) hearts (17 +/- 5% infarction) and had no effect on non-PC hearts (44 +/- 6% infarction). In prior studies we found that exogenous adenosine could substitute for ischemia to precondition the heart, indicating that adenosine is an initiator of preconditioning. These results, however, indicate that adenosine receptors must also be occupied during the long ischemic period for preconditioning to be protective and suggest that adenosine is a mediator of preconditioning as well.

Lesion of the caudal ventrolateral medulla prevents the induction of hypertension by adenosine receptor blockade in rats

2006 ◽  
Vol 1073-1074 ◽  
pp. 374-382 ◽  
Author(s):  
Dora Pinho ◽  
Teresa Sousa ◽  
Manuela Morato ◽  
Isaura Tavares ◽  
António Albino-Teixeira
Keyword(s):  
Adenosine Receptor ◽  
Ventrolateral Medulla ◽  
Receptor Blockade ◽  
Caudal Ventrolateral Medulla

Glutamate efflux from human cerebrocortical slices during ischemia: vesicular-like mode of glutamate release and sensitivity to A2A adenosine receptor blockade

2004 ◽  
Vol 47 (6) ◽  
pp. 884-891 ◽  
Author(s):  
Manuela Marcoli ◽  
Andrea Bonfanti ◽  
Paola Roccatagliata ◽  
Greta Chiaramonte ◽  
Ennio Ongini ◽  
...  
Keyword(s):  
Adenosine Receptor ◽  
Glutamate Release ◽  
Receptor Blockade ◽  
A2a Adenosine Receptor ◽  
Glutamate Efflux

Role of adenosine in norepinephrine-induced coronary vasodilation

1997 ◽  
Vol 273 (2) ◽  
pp. H557-H565 ◽  
Author(s):  
R. Van Bibber ◽  
D. W. Stepp ◽  
K. Kroll ◽  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Adenosine Receptor ◽  
Myocardial Oxygen Consumption ◽  
Temporal Correlation ◽  
Distributed Model ◽  
Receptor Blockade ◽  
Adenosine Concentration

Adenosine has been postulated to be the physiological transmitter coupling increases in coronary blood flow to increases in myocardial metabolism. The purpose of this experiment was to evaluate the role of adenosine in the coronary hyperemia due to norepinephrine. In 11 anesthetized, closed-chest canine preparations, the left main coronary artery was cannulated and perfused with blood at 100 mmHg. Coronary blood flow and myocardial oxygen consumption were measured, and interstitial adenosine concentration was estimated from arterial and coronary venous measurements using a distributed model. Adenosine receptor blockade with 8-phenyltheophylline (8-PT) was used to shift the adenosine dose-response curve 12-fold. During intracoronary norepinephrine infusion, coronary blood flow and myocardial oxygen consumption increased similarly before and after 8-PT, demonstrating a lack of an effect from the adenosine receptor blockade. Before 8-PT, estimated interstitial adenosine increased to a vasoactive concentration (220 nM); however, the temporal correlation with coronary blood flow was poor. After 8-PT, a similar increase in estimated interstitial adenosine was found, demonstrating that there was no augmentation in adenosine concentration to overcome the adenosine receptor blockade. Thus adenosine could not be responsible for the increase in coronary blood flow after adenosine receptor blockade and therefore is not required for norepinephrine-induced hyperemia.

Hypoxia-induced vasodilation of the feline superior mesenteric artery is not adenosine mediated

1990 ◽  
Vol 259 (4) ◽  
pp. G605-G610 ◽  
Author(s):  
L. K. Lockhart ◽  
W. W. Lautt
Keyword(s):  
Superior Mesenteric Artery ◽  
Vascular Resistance ◽  
Hollow Fiber ◽  
Adenosine Receptor ◽  
Mesenteric Artery ◽  
Receptor Blockade ◽  
Pentobarbital Sodium ◽  
Endogenous Adenosine ◽  
Similar Decrease

The role of adenosine in hypoxia-induced vasodilation was examined in the intestine of pentobarbital sodium-anesthetized cats. A hollow-fiber fetal oxygenator was used to selectively reduce the PO2 of the blood supplying the superior mesenteric artery, thereby inducing hypoxia in the intestines. Decreasing the PO2 from 109 to 38 Torr caused vascular resistance to decrease from 10.2 to 7.5 Torr.kg.min.ml-1, a decrease of 2.7 Torr.kg.min.ml-1 or 24%. During selective adenosine receptor blockade with 8-phenyltheophylline, the same decrease in PO2 (from 109 to 40 Torr) produced a similar decrease in resistance from 5.7 to 3.4 Torr.kg.min.ml-1 or a difference of 2.3 Torr.kg.min.ml-1 (-36%). Thus adenosine is not the mediator of hypoxia-induced vasodilation in the feline intestine because blockade of the vasodilating effects of exogenous and presumably endogenous adenosine did not affect the observed decrease in resistance.

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