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Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine

Division of Renal and Cardiovascular Research, Department of Medical Physiology, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen N, Denmark

Submitted 14 January 2003 ; accepted in final form 11 September 2003

The aim of the present study was to investigate the role of Ca²⁺-activated Cl^- channels in the renal vasoconstriction elicited by angiotensin II (ANG II) and norepinephrine (NE). Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry. Ratiometric photometry of fura 2 fluorescence was used to estimate intracellular free Ca²⁺ concentration ([Ca²⁺]_i) in isolated preglomerular vessels from rat kidneys. Renal arterial injection of ANG II (2-4 ng) and NE (20-40 ng) produced a transient decrease in RBF. Administration of ANG II (10^-7 M) and NE (5 x 10^-6 M) to the isolated preglomerular vessels caused a prompt increase in [Ca²⁺]_i. Renal preinfusion of DIDS (0.6 and 1.25 µmol/min) attenuated the ANG II-induced vasoconstriction to 35% of the control response, whereas the effects of NE were unaltered. Niflumic acid (0.14 and 0.28 µmol/min) and 2-[(2-cyclopentenyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1H-inden-5-yl)oxy]acetic acid (IAA-94; 0.045 and 0.09 µmol/min) did not affect the vasoconstrictive responses of these compounds. Pretreatment with niflumic acid (50 µM) or IAA-94 (30 µM) for 2 min decreased baseline [Ca²⁺]_i but did not change the magnitude of the [Ca²⁺]_i response to ANG II and NE in the isolated vessels. The present results do not support the hypothesis that Ca²⁺-activated Cl^- channels play a crucial role in the hemodynamic effects of ANG II and NE in rat renal vasculature.

microcirculation; vascular smooth muscle; 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid; niflumic acid; calcium channels

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