Segment-specific effect of chloride channel blockade on rat renal arteriolar contractile responses to angiotensin II

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Abstract

Experiments were performed to determine the effect of a chloride channel blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasoconstrictor responses to angiotensin II (AngII). The in vitro blood-perfused juxtamedullary nephron technique was exploited to provide access to the renal microvasculature of enalaprilat-treated rats. Under control conditions, 1 to 100 nmol/L AngII evoked concentration-dependent afferent arteriolar vasoconstriction. Baseline diameter of afferent arterioles was not altered by 30 μmol/L IAA-94; however, AngII responsiveness was markedly attenuated. The afferent response to K-induced depolarization was sustained in the presence of IAA-94. In efferent arterioles, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced afferent (but not efferent) arteriolar vasoconstriction requires participation of chloride channels, which likely engender depolarization and subsequent opening of voltage-gated calcium channels.

Original languageEnglish (US)
Pages (from-to)90-94
Number of pages5
JournalAmerican Journal of Hypertension
Volume8
Issue number1
DOIs
StatePublished - Jan 1995

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Chloride Channels
Angiotensin II
Kidney
Arterioles
Vasoconstriction
Enalaprilat
Nephrons
Vasoconstrictor Agents
Calcium Channels
Microvessels
MK 473

Keywords

  • Angiotensin II
  • arterioles
  • chloride channels
  • indanyloxyacetic acid
  • renal circulation

ASJC Scopus subject areas

  • Internal Medicine

Cite this

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title = "Segment-specific effect of chloride channel blockade on rat renal arteriolar contractile responses to angiotensin II",
abstract = "Experiments were performed to determine the effect of a chloride channel blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasoconstrictor responses to angiotensin II (AngII). The in vitro blood-perfused juxtamedullary nephron technique was exploited to provide access to the renal microvasculature of enalaprilat-treated rats. Under control conditions, 1 to 100 nmol/L AngII evoked concentration-dependent afferent arteriolar vasoconstriction. Baseline diameter of afferent arterioles was not altered by 30 μmol/L IAA-94; however, AngII responsiveness was markedly attenuated. The afferent response to K-induced depolarization was sustained in the presence of IAA-94. In efferent arterioles, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced afferent (but not efferent) arteriolar vasoconstriction requires participation of chloride channels, which likely engender depolarization and subsequent opening of voltage-gated calcium channels.",
keywords = "Angiotensin II, arterioles, chloride channels, indanyloxyacetic acid, renal circulation",
author = "Carmines, {Pamela K}",
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AU - Carmines, Pamela K

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N2 - Experiments were performed to determine the effect of a chloride channel blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasoconstrictor responses to angiotensin II (AngII). The in vitro blood-perfused juxtamedullary nephron technique was exploited to provide access to the renal microvasculature of enalaprilat-treated rats. Under control conditions, 1 to 100 nmol/L AngII evoked concentration-dependent afferent arteriolar vasoconstriction. Baseline diameter of afferent arterioles was not altered by 30 μmol/L IAA-94; however, AngII responsiveness was markedly attenuated. The afferent response to K-induced depolarization was sustained in the presence of IAA-94. In efferent arterioles, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced afferent (but not efferent) arteriolar vasoconstriction requires participation of chloride channels, which likely engender depolarization and subsequent opening of voltage-gated calcium channels.

AB - Experiments were performed to determine the effect of a chloride channel blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasoconstrictor responses to angiotensin II (AngII). The in vitro blood-perfused juxtamedullary nephron technique was exploited to provide access to the renal microvasculature of enalaprilat-treated rats. Under control conditions, 1 to 100 nmol/L AngII evoked concentration-dependent afferent arteriolar vasoconstriction. Baseline diameter of afferent arterioles was not altered by 30 μmol/L IAA-94; however, AngII responsiveness was markedly attenuated. The afferent response to K-induced depolarization was sustained in the presence of IAA-94. In efferent arterioles, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced afferent (but not efferent) arteriolar vasoconstriction requires participation of chloride channels, which likely engender depolarization and subsequent opening of voltage-gated calcium channels.

KW - Angiotensin II

KW - arterioles

KW - chloride channels

KW - indanyloxyacetic acid

KW - renal circulation

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