| 10495853 |
Hashimoto S: [The in vivo role of vascular chloride channels in the regulation of glomerular hemodynamics]. Hokkaido Igaku Zasshi. 1999 Sep;74(5):387-94.
The calcium (Ca2+)-dependent chloride channel (CIC) may have a crucial role in the modulation of the effects of Angiotensin II (AII) on vascular smooth muscle cell and glomerular mesangium. We examined in vivo effects of a Ca (2+)-dependent chloride channel blocker, R (+)-methylindazone indanyloxy acetic acid 94 (IAA-94), on renal and glomerular hemodynamics in rats. A small needle was inserted from the kidney surface and the renal interstitium was directly perfused first with saline, control solution. For AII group, AII-concentrations were serially 10 (-7) M, 10 (-6) M, and 10 (-5) M, and for AII and IAA-94 group, ratios of AII to IAA-94 (300 microM) the same serial concentrations. Perfusion with AII solution resulted in dose-dependent increase in renal vascular resistance (RVR), while no such elevation of RVR was observed under the perfusion with AII/IAA. To investigate the effects of Ca (2+)-dependent chloride channel on the regulatory mechanism of renal microcirculation, i.e., tubuloglomerular feed back (TGF) response, we performed micropuncture experiment. We measured proximal tubular stop-flow pressure (Psf) during the immersion of the corresponding nephron with drugs by the simultaneous perfusion of peritubular capillaries with the solutions containing AII (10 (-7) M) or AII and IAA-94 (300 microM). TGF response was significantly enhanced by AII, while the increment in TGF response was completely abolished by concomitant IAA. Immersion with IAA-94 alone caused no alteration in TGF response. These data suggest that chloride channels could modulate AII action in renal and glomerular hemodynamics. |
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