Contribution of calcium-activated potassium channels to the vasodilator effect of bradykinin in the isolated, perfused kidney of the rat

M. Rapacon, P. Mieyal, J. C. McGiff, David J Fulton, J. Quilley

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

1. NO- and prostaglandin-independent, endothelium-dependent vasodilator responses to bradykinin are attributed to release of a hyperpolarizing factor. Therefore, the contribution of K+ channels to the renal vasodilator effect of bradykinin was examined in rat perfused kidneys that were preconstricted with phenylephrine and treated with N(G)-nitro-L-arginine (L-NOARG) and indomethacin to inhibit NO and prostaglandin synthesis. 2. The non-specific K+ channel inhibitors, TEA and TBA reduced vasodilator responses to bradykinin and cromakalim but not those to nitroprusside. 3. Glibenclamide, an inhibitor of ATP-sensitive K+ channels, blocked the vasodilator response to cromakalim without affecting responses to bradykinin. 4. Charybdotoxin, a selective inhibitor of Ca2+-activated K+ channels, greatly attenuated vasodilator responses to bradykinin without affecting those to cromakalim or nitroprusside. 5. Iberiotoxin and leiurotoxin, inhibitors of large and small conductance Ca2+-activated K+ channels, respectively, were without effect on vasodilator responses to bradykinin, cromakalim or nitroprusside. 6. These results implicate K+ channels, specifically Ca2+-activated K+ channels of intermediate conductance, in the renal vasodilator effect of bradykinin and, thereby, support a role for a hyperpolarizing factor.

Original languageEnglish (US)
Pages (from-to)1504-1508
Number of pages5
JournalBritish Journal of Pharmacology
Volume118
Issue number6
DOIs
StatePublished - Jan 1 1996

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Calcium-Activated Potassium Channels
Bradykinin
Vasodilator Agents
Cromakalim
Kidney
Nitroprusside
Prostaglandins
Charybdotoxin
Endothelium-Dependent Relaxing Factors
Glyburide
Nitroarginine
Phenylephrine
Indomethacin
Arginine
Adenosine Triphosphate

Keywords

  • Bradykinin
  • Cytochrome P450
  • Hyperpolarizing factor
  • K channels
  • Renal vasodilatation

ASJC Scopus subject areas

  • Pharmacology

Cite this

Contribution of calcium-activated potassium channels to the vasodilator effect of bradykinin in the isolated, perfused kidney of the rat. / Rapacon, M.; Mieyal, P.; McGiff, J. C.; Fulton, David J; Quilley, J.

In: British Journal of Pharmacology, Vol. 118, No. 6, 01.01.1996, p. 1504-1508.

Research output: Contribution to journalArticle

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AB - 1. NO- and prostaglandin-independent, endothelium-dependent vasodilator responses to bradykinin are attributed to release of a hyperpolarizing factor. Therefore, the contribution of K+ channels to the renal vasodilator effect of bradykinin was examined in rat perfused kidneys that were preconstricted with phenylephrine and treated with N(G)-nitro-L-arginine (L-NOARG) and indomethacin to inhibit NO and prostaglandin synthesis. 2. The non-specific K+ channel inhibitors, TEA and TBA reduced vasodilator responses to bradykinin and cromakalim but not those to nitroprusside. 3. Glibenclamide, an inhibitor of ATP-sensitive K+ channels, blocked the vasodilator response to cromakalim without affecting responses to bradykinin. 4. Charybdotoxin, a selective inhibitor of Ca2+-activated K+ channels, greatly attenuated vasodilator responses to bradykinin without affecting those to cromakalim or nitroprusside. 5. Iberiotoxin and leiurotoxin, inhibitors of large and small conductance Ca2+-activated K+ channels, respectively, were without effect on vasodilator responses to bradykinin, cromakalim or nitroprusside. 6. These results implicate K+ channels, specifically Ca2+-activated K+ channels of intermediate conductance, in the renal vasodilator effect of bradykinin and, thereby, support a role for a hyperpolarizing factor.

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