Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells

Tamás L. Török, Tünde Pauló, Péter T. Tóth, Awad M. Azzidani, David A. Powis, K. Magyar

Research output: Contribution to journalArticle

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Abstract

1. 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 × 10-5 M). 2. 2. The Na+-pump inhibitor sodium-azide (NaN3, 2 mM) 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. 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. 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. 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. 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. The transmitter releasing action of azide can be antagonized by reactivation of the Na+-pump by readmission of K+ to Na+-loaded cells.

Original languageEnglish
Pages (from-to)143-149
Number of pages7
JournalGeneral Pharmacology
Volume20
Issue number2
DOIs
Publication statusPublished - 1989

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Sodium Azide
Chromaffin Cells
Peripheral Nerves
Catecholamines
Norepinephrine
Neurons
Ouabain
Azides
Arteries
Pulmonary Artery
Cocaine
Rabbits
Muscles

ASJC Scopus subject areas

  • Pharmacology

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Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells. / Török, Tamás L.; Pauló, Tünde; Tóth, Péter T.; Azzidani, Awad M.; Powis, David A.; Magyar, K.

In: General Pharmacology, Vol. 20, No. 2, 1989, p. 143-149.

Research output: Contribution to journalArticle

Török, Tamás L. ; Pauló, Tünde ; Tóth, Péter T. ; Azzidani, Awad M. ; Powis, David A. ; Magyar, K. / Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells. In: General Pharmacology. 1989 ; Vol. 20, No. 2. pp. 143-149.
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abstract = "1. 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 × 10-5 M). 2. 2. The Na+-pump inhibitor sodium-azide (NaN3, 2 mM) 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. 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. 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. 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. 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. The transmitter releasing action of azide can be antagonized by reactivation of the Na+-pump by readmission of K+ to Na+-loaded cells.",
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N2 - 1. 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 × 10-5 M). 2. 2. The Na+-pump inhibitor sodium-azide (NaN3, 2 mM) 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. 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. 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. 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. 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. The transmitter releasing action of azide can be antagonized by reactivation of the Na+-pump by readmission of K+ to Na+-loaded cells.

AB - 1. 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 × 10-5 M). 2. 2. The Na+-pump inhibitor sodium-azide (NaN3, 2 mM) 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. 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. 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. 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. 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. The transmitter releasing action of azide can be antagonized by reactivation of the Na+-pump by readmission of K+ to Na+-loaded cells.

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