title: Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells.
abstract: 1. The spontaneous release of [3H]noradrenaline [( 3H]NA) has been measured from rabbit pulmonary arteries and bovine chromaffin cells in the presence of neuronal uptake blocker cocaine (3 x 10(-5) M). 2. The Na+-pump inhibitor sodium-azide (NaN3, 2mM) produced a moderate increase of [3H]NA release from both preparations and relaxed the arteries. The [3H]releasing action of NaN3 was accompanied by a 30% inhibition of 86Rb-uptake into chromaffin cells. 3. In both preparations, ouabain (10(-4) M) markedly increased the release of [3H], contracted the arteries and inhibited the 86Rb-uptake of chromaffin cells by about 75%. A combined application of NaN3 and ouabain produced a similar inhibition of 86Rb-uptake of chromaffin cells and failed to increase further the release of [3H] in comparison to that found in response to ouabain alone. 4. Removal of K+ from the external medium increased both the release of [3H]NA and the tone of pulmonary arteries. NaN3 further increased the transmitter release in "K+-free" solution but relaxed the muscle. In the absence of external K+ and in the presence of azide, ouabain further enhanced the transmitter release but failed to produce significant contraction. 5. Reactivation of the Na+-pump by readmission of K+ (5.9 mM) to the external medium abolished the transmitter releasing action of NaN3 in arteries. 6. It is concluded that in peripheral sympathetic nerves and chromaffin cells, NaN3 inhibits the Na+-pump producing NA and CA release respectively and in nerves even if NA release had already been increased by K+-removal.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pharmacodynamics, Semmelweis University of Medicine, Budapest, Hungary.
authors.forename: T L
authors.initials: TL
authors.lastname: Török
authors.forename: T
authors.initials: T
authors.lastname: Pauló
authors.forename: P T
authors.initials: PT
authors.lastname: Tóth
authors.forename: A M
authors.initials: AM
authors.lastname: Azzidani
authors.forename: D A
authors.initials: DA
authors.lastname: Powis
authors.forename: K
authors.initials: K
authors.lastname: Magyar
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000378:metabolism; D001386:Azides / Q000494:pharmacology*; D002395:Catecholamines / Q000378:metabolism*; D002838:Chromaffin System / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D046508:Culture Techniques; D005260:Female; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D019810:Sodium Azide; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000378:metabolism*
chemical_list: D001386:Azides; D002395:Catecholamines; D010042:Ouabain; D019810:Sodium Azide; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D009638:Norepinephrine