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Angiotensin II-stimulated Ca²⁺ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na⁺/Ca²⁺ exchange

Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Submitted 25 May 2007 ; accepted in final form 26 October 2007

In afferent arterioles, the signaling events that lead to an increase in cytosolic Ca²⁺ concentration ([Ca²⁺]_i) and initiation of vascular contraction are increasingly being delineated. We have recently studied angiotensin II (ANG II)-mediated effects on sarcoplasmic reticulum (SR) mobilization of Ca²⁺ and the role of superoxide and cyclic adenosine diphosphoribose in these processes. In the current study we investigated the participation of transient receptor potential canonical channels (TRPC) and a Na⁺/Ca²⁺ exchanger (NCX) in Ca²⁺ entry mechanisms. Afferent arterioles, isolated with the magnetized polystyrene bead method, were loaded with fura-2 to measure [Ca²⁺]_i ratiometrically. We observed that the Ca²⁺-dependent chloride channel blocker niflumic acid (10 and 50 µ M) affects neither the peak nor plateau [Ca²⁺]_i response to ANG II. Arterioles were pretreated with ryanodine (100 µM) and TMB-8 to block SR mobilization via the ryanodine receptor and inositol trisphosphate receptor, respectively. The peak [Ca²⁺]_i response to ANG II was reduced by 40%. Addition of 2-aminoethoxydiphenyl borane to block TRPC-mediated Ca²⁺ entry inhibited the peak [Ca²⁺]_i ANG II response by 80% and the plateau by 74%. Flufenamic acid (FFA; 50 µM), which stimulates TRPC6, caused a sustained increase of [Ca²⁺]_i of 146 nM. This response was unaffected by diltiazem or nifedipine. KB-R7943 (at the low concentration of 10 µM) inhibits reverse (but not forward) mode NCX. KB-R7943 decreased the peak [Ca²⁺]_i response to ANG II by 48% and to FFA by 38%. We conclude that TRPC6 and reverse-mode NCX may be important Ca²⁺ entry pathways in afferent arterioles.

renal microcirculation; voltage-gated calcium entry; vascular smooth muscle cell

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