TY - JOUR
T1 - Ionic effects of angiotensin II and their role in the activation of the Na+/H+ antiporter
AU - Flores, G.
AU - Ye, M.
AU - LaPointe, M.
AU - Batlle, D.
PY - 1996/1/1
Y1 - 1996/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0030162485&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030162485&partnerID=8YFLogxK
M3 - Article
C2 - 8743531
AN - SCOPUS:0030162485
SP - S-122-S-125
JO - Kidney International, Supplement
JF - Kidney International, Supplement
SN - 0098-6577
IS - 55
ER -