Chloride is essential for contraction of afferent arterioles after
agonists and potassium.
Jensen, Boye L., Peter Ellekvist, and Ole Sktt.
Institute of Medical Physiology, University of Copenhagen, Denmark,
and Department of Physiology, University of Odense, Denmark
APStracts 3:0225F, 1996.
A depolarizing chloride efflux has been suggested to activate voltage
-dependent calcium channels in renal afferent arteriolar smooth muscle
cells in response to vasoconstrictors. To test this proposal rabbit
afferent arterioles were microperfused, and the contractile dose
-responses to norepinephrine, angiotensin II and potassium were
measured after chloride-depletion, and compared to controls. Chloride
depletion did not change arteriolar diameters, but the response to
norepinephrine was markedly reduced, when chloride was substituted
with gluconate (n=6) or isethionate (n=6). Reintroduction of chloride
fully restored the sensitivity to norepinephrine. Contractions after
angiotensin II and potassium were totally abolished in the absence of
chloride (n=6). In additional experiments (n=7) the arteriolar
contraction to 100 mM potassium was abolished after only 1 min
removal of extracellular chloride.. We conclude that norepinephrine
and angiotensin II use different mechanisms- for contraction, and
that extracellular chloride is essential for contraction in afferent
arterioles after activation of voltage-dependent calcium channels. We
suggest that a chloride influx-pathway is activated concomitantly
with the voltage-dependent calcium channel to allow chloride influx
to compensate for the cation influx.
Received 16 May 1996; accepted in final form 5 December 1996.
APS Manuscript Number F152-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996