Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were performed on isolated, nonworking rat hearts perfused at constant pressure according to the Langendorff technique to evaluate the role of adenosine in hypercapnia-evoked coronary vasodilation. Hypercapnia/acidosis resulted in increases in heart rate and coronary flow rates in conjunction with a decrease in ventricular contractile tensions. The adenosine deaminase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA, 10 microM) reduced the heart rate and enhanced CO2-evoked increases in coronary vascular flow. 5-Iodotubercidin (1 microM), an inhibitor of adenosine kinase, caused a reduction in heart rate and enhanced coronary flow rates during hypercapnic perfusion. Adenosine deaminase (1 U/ml) significantly attenuated CO2-evoked increases in coronary vascular flow. These results extend those of previous investigations implicating adenosine in the regulation of coronary flow during conditions of respiratory or metabolic acidosis.
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PMID:Further evidence for the role of adenosine in hypercapnia/acidosis-evoked coronary flow regulation. 1055 85

Adenosine is one of the most important neuromodulators in the CNS, both under physiological and pathological conditions. In the isolated spinal cord of the neonatal rat in vitro, acute hypercapnic acidosis (20% CO2, pH 6.7) reversibly depressed electrically evoked spinal reflex potentials. This depression was partially reversed by 8-cyclopentlyl-1,3-dimethylxanthine (CPT), a selective A1 adenosine receptor antagonist. Isohydric hypercapnia (20% CO2, pH 7.3), but not isocapnic acidosis (5% CO2, pH 6.7), depressed the reflex potentials, which were also reversed by CPT. An ecto-5'-nucleotidase inhibitor did not affect the hypercapnic acidosis-evoked depression. An inhibitor of adenosine kinase, but not deaminase, mimicked the inhibitory effect of hypercapnic acidosis on the spinal reflex potentials. Accumulation of extracellular adenosine and inhibition of adenosine kinase activity were caused by hypercapnic acidosis and isohydric hypercapnia, but not isohydric acidosis. These results indicate that the activation of adenosine A1 receptors is involved in the hypercapnia-evoked depression of reflex potentials in the isolated spinal cord of the neonatal rat. The inhibition of adenosine kinase activity is suggested to cause the accumulation of extracellular adenosine during hypercapnia.
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PMID:Involvement of adenosine in depression of synaptic transmission during hypercapnia in isolated spinal cord of neonatal rats. 1677 47