Possible involvement of both N- and L-type voltage-dependent Ca channels in adrenergic neurotransmission of canine saphenous veins in low Ca2+ plus tetraethylammonium medium
| Autor: | Junko Ozawa, Hitoshi Kato, Yoshinobu Takata |
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| Rok vydání: | 1992 |
| Předmět: |
Agonist
Dihydropyridines medicine.medical_specialty medicine.drug_class chemistry.chemical_element Adrenergic Calcium Neurotransmission Synaptic Transmission Muscle Smooth Vascular chemistry.chemical_compound Dogs Nifedipine Internal medicine medicine Animals Nisoldipine Saphenous Vein Pharmacology Tetraethylammonium Dihydropyridine General Medicine Tetraethylammonium Compounds Calcium Channel Blockers Endocrinology chemistry Calcium Channels Adrenergic Fibers medicine.drug |
| Zdroj: | Naunyn-Schmiedeberg's Archives of Pharmacology. 346 |
| ISSN: | 1432-1912 0028-1298 |
| DOI: | 10.1007/bf00171084 |
| Popis: | The involvement of N- and L-type voltage-dependent Ca channels (VDCCs) in adrenergic neurotransmission under the superfusion with 0.25 mM Ca2+ + 20 mM tetraethylammonium (low Ca2+ + TEA) medium has been studied by examining the effects of ω-conotoxin GVIA (ω-CTX) and dihydropyridine antagonists and agonist on transmural nerve stimulation (TNS)-evoked 3H overflow from canine saphenous veins preloaded with [3H]-noradrenaline. Nisoldipine (10 and 30 μM) and nifedipine (30 μM) reduced significantly the TNS-evoked 3H overflow in low Ca2+ + TEA medium, while the two dihydropyridine antagonists failed to suppress it in normal Krebs medium. Bay K 8644 (30 and 100 nM) produced a significant and concentration-dependent enhancement of the TNS-evoked 3H overflow in low Ca2+ + TEA medium. The enhancing effects of Bay K 8644 were antagonized by both 3 μM nisoldipine and 10 μtM nifedipine. ω-CTX inhibited markedly the TNS-evoked 3H overflow in both normal Krebs and low Ca2+ + TEA media, the inhibition by ω-CTX being ten times more potent in low Ca2+ + TEA medium. Nisoldipine (30 μM), when combined with 1 nM ω-CTX, produced a further significant inhibition of the TNS-evoked 3H overflow in low Ca2+ + TEA medium. However, no additional inhibition by 30 μM nisoldipine was observed when ω-CTX concentration was raised to 2 nM. In the veins superfused with normal Krebs medium, nisoldipine (30 μM) did not affect the inhibitory effect of 10 nM ω-CTX on the evoked 3H overflow. The low Ca2+ + TEA medium increased the spontaneous 3H overflow, which was not influenced by ω-CTX and dihydropyridines. These results suggest that in low Ca2+ + TEA medium but not normal Krebs one, Ca2+ entry via both N- and L-type VDCCs may be involved in adrenergic neurotransmission in the canine saphenous veins. |
| Databáze: | OpenAIRE |
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