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. 1988 Jun;94(2):355–362. doi: 10.1111/j.1476-5381.1988.tb11537.x

Differential effect of omega-conotoxin on release of the adrenergic transmitter and the vasoconstrictor response to noradrenaline in the rat isolated kidney.

M M el-Din 1, K U Malik 1
PMCID: PMC1853999  PMID: 2456115

Abstract

1. The effects of the Ca2+ channel blockers omega-conotoxin (omega-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 [3H]-noradrenaline ([3H]-NA). 2. RNS (1-4 Hz), Vt (15-90 nmol) and KCl (150-500 mumol) produced renal vasoconstriction and enhanced the tritium overflow in a frequency- and concentration-dependent manner, respectively. 3. Administration of omega-CgTx (50 nM) 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, omega-CgTx failed to alter the vasoconstrictor response elicited by exogenous NA. 4. Infusion of nifedipine (10 microM) enhanced the tritium overflow elicited by RNS and KCl but not by Vt; a low dose of nifedipine (1.4 microM) enhanced the tritium overflow elicited by all these stimuli. Low doses of diltiazem (6 microM) failed to alter the tritium overflow produced by these stimuli. However, higher doses of diltiazem (60 microM) reduced the tritium overflow elicited 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.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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