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Differential effect of ω‐conotoxin on release of the adrenergic transmitter and the vasoconstrictor response to noradrenaline in the rat isolated kidney
Author(s) -
ElDin Mahmoud m. Mohy,
Malik Kafait U.
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11537.x
Subject(s) - nifedipine , chemistry , vasoconstriction , diltiazem , veratridine , medicine , endocrinology , kidney , tritium , stimulation , calcium , sodium , sodium channel , physics , organic chemistry , nuclear physics
1 The effects of the Ca 2+ channel blockers ω‐conotoxin (ω‐CgTx), nifedipine and diltiazem, on the increase in tritium overflow and perfusion pressure elicited by renal nerve stimulation (RNS), veratridine (Vt) and potassium chloride (KCl), and on the vasoconstrictor response produced by noradrenaline (NA) were investigated in the isolated kidney of the rat perfused with Tyrode solution and prelabelled with [ 3 H]‐noradrenaline ([ 3 H]‐NA). 2 RNS (1–4Hz), Vt (15–90 nmol) and KCl (150–500 μmol) produced renal vasoconstriction and enhanced the tritium overflow in a frequency‐ and concentration‐dependent manner, respectively. 3 Administration of ω‐CgTx (50 n m ) inhibited RNS‐, Vt‐ and KCl‐induced overflow of tritium; the associated renal vasoconstriction produced by RNS or Vt but not by KCl was inhibited. In contrast, ω‐CgTx failed to alter the vasoconstrictor response elicited by exogenous NA. 4 Infusion of nifedipine (10 μ m ) enhanced the tritium overflow elicited by RNS and KCl but not by Vt; a low dose of nifedipine (1.4 μ m ) enhanced the tritium overflow elicited by all these stimuli. Low doses of diltiazem (6 μ m ) failed to alter the tritium overflow produced by these stimuli. However, higher doses of diltiazem (60 μ m ) reduced the tritium overflow elicted by RNS or Vt but enhanced that caused by KCl. The renal vasoconstriction produced by RNS, Vt and KCl as well as by exogenous NA was inhibited by low and high doses of nifedipine and diltiazem. 5 These data suggest that (a) RNS, Vt and KCl enhance the release of adrenergic transmitter by promoting the influx of Ca 2+ into the nerve terminal through specific Ca 2+ channels, probably N‐type Ca 2+ channels that are distinct from those located in the vascular smooth muscle and (b) ω‐CgTx could be a useful tool to differentiate between Ca 2+ channels at the adrenergic nerve terminal and vascular smooth muscle.