title: Ionic mechanism of action of adenosine on the rat superior cervical ganglion.
abstract: 1. The ionic mechanism responsible for hyperpolarization of the rat superior cervical ganglion (SCG) and depression of the depolarizing response to muscarine by adenosine was studied using an extracellular grease-gap recording technique. 2. Both the hyperpolarizations to adenosine and 2-chloroadenosine and the depression of the response to muscarine by adenosine were potentiated in reduced external calcium (Ca2+). Hyperpolarizations to adenosine were either unaltered or potentiated in the presence of the dihydropyridine Ca2+ channel antagonists, nitrendipine or (+)PN200 110 respectively. Hyperpolarizations to adenosine were unaltered by inorganic Ca2+ channel antagonists except for cobalt, which also antagonized hyperpolarizations to carbachol and depolarizations to muscarine. 3. Hyperpolarizations to adenosine were unaltered in nominally magnesium (Mg2+)-free or in reduced external chloride (Cl-) media. When sodium ions (Na+) were replaced by lithium ions (Li+) maximal responses to adenosine were initially enhanced, returning to pretreatment levels and subsequently reduced in their duration. In contrast, responses to adenosine were significantly enhanced in nominally potassium (K+)-free medium and reduced upon doubling the extracellular K+. 4. Hyperpolarizations were enhanced in the presence of the K+ channel antagonists, 4-aminopyridine and 3,4-diaminopyridine, and reduced by a low concentration (2 mM) of tetraethylammonium (TEA), but not in 10 mM TEA. 5. The results support the hypothesis that adenosine-mediated hyperpolarization of postganglionic neurones of the rat SCG is by a Ca(2+)-independent mechanism and is probably mediated via an increase of a K+ current. The results also indicate that adenosine-induced hyperpolarizations of the rat SCG are independent of the presence of extracellular magnesium.
authors.affiliation: Department of Pharmacology, Glasgow University, UK.
authors.forename: G P
authors.initials: GP
authors.lastname: Connolly
authors.forename: T W
authors.initials: TW
authors.lastname: Stone
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001464:Barium / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D016764:Cell Polarity / Q000187:drug effects / Q000502:physiology; D018118:Chloride Channels / Q000502:physiology; D003864:Depression, Chemical; D005110:Extracellular Space / Q000737:chemistry; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology; D008094:Lithium / Q000494:pharmacology; D008274:Magnesium / Q000378:metabolism; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009116:Muscarine / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D011976:Receptors, Muscarinic / Q000502:physiology; D017783:Superior Cervical Ganglion / Q000187:drug effects* / Q000502:physiology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D018118:Chloride Channels; D007473:Ion Channels; D015221:Potassium Channels; D011976:Receptors, Muscarinic; D001464:Barium; D010042:Ouabain; D009116:Muscarine; D008094:Lithium; D008274:Magnesium; D000241:Adenosine; D011188:Potassium; D002118:Calcium