Blockade of chloride channels by DIDS stimulates renin release and inhibits contraction of afferent arterioles

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.
Original languageEnglish
JournalAmerican Journal of Physiology (Consolidated)
Volume270
Issue number5 Pt 2
Pages (from-to)F718-27
ISSN0002-9513
Publication statusPublished - 1996

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Renin
Acids
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Rabbits
Ethylene Glycol
Ether
Kidney

Keywords

  • 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
  • Angiotensin II
  • Animals
  • Arterioles
  • Chloride Channels
  • Juxtaglomerular Apparatus
  • Male
  • Norepinephrine
  • Perfusion
  • Rabbits
  • Rats
  • Rats, Sprague-Dawley
  • Renin
  • Vasoconstriction

Cite this

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title = "Blockade of chloride channels by DIDS stimulates renin release and inhibits contraction of afferent arterioles",
abstract = "Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.",
keywords = "4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid, Angiotensin II, Animals, Arterioles, Chloride Channels, Juxtaglomerular Apparatus, Male, Norepinephrine, Perfusion, Rabbits, Rats, Rats, Sprague-Dawley, Renin, Vasoconstriction",
author = "Jensen, {B L} and O Sk{\o}tt",
year = "1996",
language = "English",
volume = "270",
pages = "F718--27",
journal = "American Journal of Physiology (Consolidated)",
issn = "0002-9513",
publisher = "American Physiological Society",
number = "5 Pt 2",

}

Blockade of chloride channels by DIDS stimulates renin release and inhibits contraction of afferent arterioles. / Jensen, B L; Skøtt, O.

In: American Journal of Physiology (Consolidated), Vol. 270, No. 5 Pt 2, 1996, p. F718-27.

Research output: Contribution to journalJournal articleResearchpeer-review

TY - JOUR

T1 - Blockade of chloride channels by DIDS stimulates renin release and inhibits contraction of afferent arterioles

AU - Jensen, B L

AU - Skøtt, O

PY - 1996

Y1 - 1996

N2 - Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.

AB - Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.

KW - 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid

KW - Angiotensin II

KW - Animals

KW - Arterioles

KW - Chloride Channels

KW - Juxtaglomerular Apparatus

KW - Male

KW - Norepinephrine

KW - Perfusion

KW - Rabbits

KW - Rats

KW - Rats, Sprague-Dawley

KW - Renin

KW - Vasoconstriction

M3 - Journal article

VL - 270

SP - F718-27

JO - American Journal of Physiology (Consolidated)

JF - American Journal of Physiology (Consolidated)

SN - 0002-9513

IS - 5 Pt 2

ER -