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Myocardial adenosine stimulates release of cyclic adenosine monophosphate from capillary endothelial cells in guinea pig heart.
Pflugers Arch
May 1993
Center for Bioengineering, University of Washington, Seattle 98195.
Activation of coronary endothelial cell adenylate cyclase was studied in the isolated guinea pig heart by prelabelling endothelial adenine nucleotides using intracoronary infusion of [3H]-adenosine, and measuring the coronary efflux of [3H]-cyclic adenosine monophosphate (cAMP). Hypoxia (30% O2) caused a 4-fold increase in coronary release of [3H]-cAMP, which was decreased by 63% by infusion of the adenosine receptor antagonist, theophylline (50 microM). During normoxic control conditions, degrading adenosine to non-vasoactive inosine by intracoronary infusion of adenosine deaminase (1.
View Article and Find Full Text PDFInosine transiently decreases coronary flow but potentiates vasodilation by adenosine.
Am J Physiol
September 1990
Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
To test whether inosine interferes with the action of adenosine, we investigated the effects of intracoronary administration of inosine, adenosine, 8-phenyltheophylline, and adenosine deaminase on isolated rat heart. Inosine did not change heart rate or developed tension but increased the effluent adenosine concentration. Inosine also decreased exogenous adenosine uptake and breakdown.
View Article and Find Full Text PDFAdenosine is unimportant in controlling coronary blood flow in unstressed dog hearts.
Am J Physiol
December 1985
The adenosine hypothesis of local metabolic control of coronary blood flow was tested in the unstressed heart with adenosine deaminase, which converts adenosine to nonvasoactive inosine. If adenosine is normally an important physiological regulator, then adenosine deaminase should lower coronary blood flow. The left main coronary artery was perfused at constant pressure in anesthetized, closed-chest dogs.
View Article and Find Full Text PDFEffect of topical adenosine deaminase treatment on the functional hyperemic and hypoxic responses of cerebrocortical microcirculation.
J Cereb Blood Flow Metab
September 1984
The purpose of this study was to investigate the possible importance of adenosine in cerebrocortical vasodilatation accompanying brain activation (epileptic seizures and direct electrical stimulation) and hypoxia (arterial hypoxia and cyanide poisoning of the brain cortex). In chloralose-anesthetized cats a circumscribed area of the brain cortex was treated with adenosine deaminase (Type III; Sigma), which potently deaminates adenosine to the nonvasoactive inosine. Cerebrocortical vascular volume and fluorescence of reduced nicotinamide adenine dinucleotide were measured in vivo by surface fluororeflectometry.
View Article and Find Full Text PDFDuring contraction of skeletal muscle in the isolated dog hindlimb under constant-flow perfusion, the specific activity of infused [8- 14C]adenosine (nonvasoactive concn) in venous effluents decreased to 7% of the resting level in 1.25 min and was associated with a concomitant decrease in vascular resistance to 39% of the resting value. Since this decrease in specific activity of labeled adenosine could have been due to 1) an enhanced adenosine release by parenchymal tissue, 2) an exercise-induced increase in the number of open capillaries (greater surface area) in the absence of increased adenosine production 3) some degree of tissue hypoxia, or 4) a combination of these factors, experiments with maximally dilated vessels were performed.
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