Fig. 1. Representative recordings of the effect of 1 μm angiotensin II (AngII) on intracellular Ca2+increase in a control cell from WKY and in cells incubated in the presence of 1, 2, or 3% isoflurane. In protocols A –D , cells were exposed to AngII in the presence of external Ca2+(Cao2+). In protocols E –H , cells were incubated for 60 s in the nominal absence of external Ca2+and then exposed to Ang II. External Ca2+was reintroduced in the perfusion medium and AngII-induced Ca2+influx was estimated by the time course of Ca2+increase. In recordings B –D  and F –H , cells were incubated in Na+–HEPES medium containing 1, 2, and 3% isoflurane, respectively (15 min). Ratios of the emission fluorescence (> 520 nm) measured at excitation wavelengths of 350 and 380 nm are shown on the ordinate.

Fig. 1. Representative recordings of the effect of 1 μm angiotensin II (AngII) on intracellular Ca2+increase in a control cell from WKY and in cells incubated in the presence of 1, 2, or 3% isoflurane. In protocols A –D , cells were exposed to AngII in the presence of external Ca2+(Cao2+). In protocols E –H , cells were incubated for 60 s in the nominal absence of external Ca2+and then exposed to Ang II. External Ca2+was reintroduced in the perfusion medium and AngII-induced Ca2+influx was estimated by the time course of Ca2+increase. In recordings B –D  and F –H , cells were incubated in Na+–HEPES medium containing 1, 2, and 3% isoflurane, respectively (15 min). Ratios of the emission fluorescence (> 520 nm) measured at excitation wavelengths of 350 and 380 nm are shown on the ordinate.

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