Kidney and Blood Pressure Research
Original Paper
Chloride Channel Blockade Attenuates the Effect of Angiotensin II on Tubuloglomerular Feedback in WKY but not Spontaneously Hypertensive RatsHashimoto S.a · Kawata T.a · Schnermann J.b · Koike T.aaDepartment of Internal Medicine II, Hokkaido University School of Medicine, Kita-ku, Sapporo, Japan; bNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, MSC 1370, Bethesda,Md., USA
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Article / Publication Details
Received: May 20, 2003
Accepted: August 21, 2003
Published online: February 02, 2004
Issue release date: July 2004
Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 1
ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)
For additional information: https://www.karger.com/KBR
Abstract
Recent studies have shown that calcium-dependent chloride channels may play a crucial role in the modulation of the vascular effects of angiotensin II (ANG II). Thus, alterations in the function of these channels may be responsible for the enhanced renal vasoconstrictor and tubuloglomerular feedback (TGF) response to ANG II in spontaneously hypertensive rats (SHR). We investigated the effect of the calcium-dependent chloride channel blocker IAA-94 on renal hemodynamics and TGF responses. The renal interstitium was perfused with control solution, with ANG II, and with both ANG II and IAA-94. In Wistar Kyoto rats (WKY), perfusion with ANG II significantly increased renal vascular resistance (RVR), but the effect was significantly attenuated by perfusion with ANG II/IAA-94. In SHR, ANG II caused a significant elevation of RVR that was not altered by the simultaneous infusion of IAA-94. Proximal tubular stop flow pressure (Psf) was monitored during perfusion of peritubular capillaries with control solution, and subsequently with IAA-94, ANG II or both ANG II and IAA-94. TGF response magnitude of WKY rats was significantly augmented with ANG II, and this effect was suppressed by perfusion with ANG II /IAA-94. However, in SHR peritubular perfusion with ANG II/IAA-94 did not suppress the TGF response. We conclude that chloride channels susceptible to IAA-94 may play a significant role in modulating the effects of ANG II on renal hemodynamics, and that this modulation is absent in SHR.
© 2004 S. Karger AG, Basel
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Article / Publication Details
Received: May 20, 2003
Accepted: August 21, 2003
Published online: February 02, 2004
Issue release date: July 2004
Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 1
ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)
For additional information: https://www.karger.com/KBR
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