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.

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 omega-conotoxin GVIA (omega-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 microM) and nifedipine (30 microM) 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 microM nisoldipine and 10 microM nifedipine. omega-CTX inhibited markedly the TNS-evoked 3H overflow in both normal Krebs and low Ca2+ + TEA media, the inhibition by omega-CTX being ten times more potent in low Ca2+ + TEA medium. Nisoldipine (30 microM), when combined with 1 nM omega-CTX, produced a further significant inhibition of the TNS-evoked 3H overflow in low Ca2+ + TEA medium. However, no additional inhibition by 30 microM nisoldipine was observed when omega-CTX concentration was raised to 2 nM. In the veins superfused with normal Krebs medium, nisoldipine (30 microM) did not affect the inhibitory effect of 10 nM omega-CTX on the evoked 3H overflow.(ABSTRACT TRUNCATED AT 250 WORDS)