Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelium-derived relaxing factor [EDRF, nitric oxide (NO) or a NO-containing compound] influences basal tone of cerebral blood vessels and mediates vasodilation in response to several stimuli. It is not known whether EDRF also modulates responses to cerebral vasoconstrictor stimuli in vivo. Our goal was to determine whether formation of EDRF inhibits constrictor responses of large cerebral arteries to serotonin. We measured cerebral blood flow (microspheres) and pial microvascular pressure (servo null) in anesthetized rabbits and calculated resistance of large cerebral arteries. Responses to an inhibitor of NO formation, NG-nitro-L-arginine (L-NNA, 3 mg/kg i.v.), were examined. L-NNA produced an increase in resistance of large arteries and total cerebral vascular resistance of approximately 15% (p less than 0.05 for both variables) and a small decrease in cerebral blood flow (35 +/- 9 vs. 32 +/- 7 ml min-1 100 g-1, mean +/- SD, p less than 0.05). Under control conditions, infusion of serotonin (10 micrograms kg-1 min-1, into the left atrium) produced an increase in resistance of large arteries. Following treatment with L-NNA, the change in resistance of large arteries in response to serotonin was increased more than twofold (0.20 +/- 0.17 vs. 0.43 +/- 0.21 mm Hg ml-1 min 100 g, p less than 0.05). In contrast, L-NNA did not alter the increase in resistance of large arteries during hypocapnia. L-arginine inhibited the effects of L-NNA on baseline cerebral vascular resistance and on responses of large arteries to serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelium-derived relaxing factor inhibits constrictor responses of large cerebral arteries to serotonin. 156 43

The role of the L-arginine-nitric oxide (NO) system, the role of the endogenous morphine-like substances (endorphins), and the possible interaction between these two systems in the modulation of regional cerebral and spinal CO2 responsiveness was investigated in anesthetized, ventilated, normotensive, normoxic cats. Regional cerebral blood flow was measured with radiolabeled microspheres in hypocapnic, normocapnic, and hypercapnic conditions in nine individual cerebral and spinal cord regions. General opiate receptor blockade by 1 mg/kg naloxone intravenously alone or NO synthase blockade by 3 mg/kg N(omega)-nitro-L-arginine-methyl ester (L-NAME) intravenously alone caused no changes in regional CO2 responsiveness. Combined administration of these two blocking agents in the very same doses, however, resulted in a strong potentiation, with a statistically significant reduction of the CO2 responsiveness observed. Separation of the blood flow response to hypercapnia and hypocapnia indicates that this reduction occurs only during hypercapnia. Specific mu and delta opiate receptors were blocked by 0.5 mg kg(-1) IV beta-funaltrexamine and 0.4 mg kg(-1) IV naltrindole, respectively. The role of specific mu and delta opiate receptors in the NO-opiate interaction was found to be negligible because neither mu nor delta receptor blockade along with simultaneous NO blockade were able to decrease CO2 responsiveness. The current findings suggest a previously unknown interaction between the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) system and the endogenous opiate system in the cerebrovascular bed during hypercapnic stimulation, with the phenomenon not mediated by mu or delta opiate receptors.
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PMID:Interactions between the endothelium-derived relaxing factor/nitric oxide system and the endogenous opiate system in the modulation of cerebral and spinal vascular CO2 responsiveness. 1148 29