The possible interdependence of the effects of angiotensin II (Ang II) on intracellular pH (pH(i)), free cytosolic calcium (Ca(i)2+) and free cytosolic sodium (Na(i)+) was studied in cultured vascular smooth muscle cells (VSMC) from rat aorta. Cells were loaded with either BCECF/AM, SBFI/AM or Fura-2 for measurement of pH(i), Na(i)+ or Ca(i)2+, respectively. Superfusing with a HEPES solution containing Ang II (1 μM) caused a progressive increase in Na(i)+. Concurrent pH(i) changes measured in parallel experiments showed that Ang II caused a brief cell acidification followed by a delayed alkalinization, which is due to activation of the Na+/H+ antiporter. Concurrent Ca(i)2+ changes measured in parallel experiments showed that Ang II caused a prompt rise in Ca(i)2+ with a peak response at ~30 seconds followed by a rapid recovery. Obliteration of the Ang II-induced rise in Ca(i)2+ using a Ca2+ chelator (BAPTA), prevented the initial cell acidification but did not prevent the delayed rise in pH(i), which reflects stimulation of the Na+/H- antiporter. Our data thus show that in cultured VSMC neither the rise in Ca(i)2+ nor the fall in pH(i) caused by Ang II is a total prerequisite for activation of the Na+/H+ antiporter by this agonist.
|Original language||English (US)|
|Journal||Kidney International, Supplement|
|State||Published - Jan 1 1996|
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