caa a22 4500 469078332 CHVBK 20180323132941.0 cr unu---uuuuu 170328e19921001xx s 000 0 eng 10.1007/BF00171084 doi (NATIONALLICENCE)springer-10.1007/BF00171084 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 [Elektronische Daten] [Yoshinobu Takata, Junko Ozawa, Hitoshi Kato] Summary: 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. Springer-Verlag, 1992 Canine saphenous veins nationallicence Adrenergic neurotransmission nationallicence N- and L-type voltage-dependent Ca channels nationallicence Ca antagonists nationallicence Low Ca2+ + tetraethylammonium medium nationallicence Takata Yoshinobu Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, 199-01, Sagamiko, Kanagawa, Japan aut Ozawa Junko Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, 199-01, Sagamiko, Kanagawa, Japan aut Kato Hitoshi Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, 199-01, Sagamiko, Kanagawa, Japan aut Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 346/4(1992-10-01), 419-424 0028-1298 346:4<419 1992 346 210 https://doi.org/10.1007/BF00171084 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00171084 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Takata Yoshinobu Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, 199-01, Sagamiko, Kanagawa, Japan aut NATIONALLICENCE 700 1- Ozawa Junko Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, 199-01, Sagamiko, Kanagawa, Japan aut NATIONALLICENCE 700 1- Kato Hitoshi Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, 199-01, Sagamiko, Kanagawa, Japan aut NATIONALLICENCE 773 0- Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 346/4(1992-10-01), 419-424 0028-1298 346:4<419 1992 346 210 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer