Background:
Angiotensin ii (ang ii) action on h+-atpase is not clearly defined, and may vary with renal tubule segment and hormonal doses being studied. since an increase of cytosolic calcium ([ca2+]i) can stimulate acid vesicle movement and exocytotic insertion of proton pumps, and it has been shown that ang ii increases [ca2+]i while atrial natriuretic peptide (anp) reduces it, there may be some interaction between ang ii and anp in the regulation of intracellular ph (phi) mediated by h+-atpase.
Methods:
The effects of ang ii and/or anp on the regulation of phi via h+-atpase and of [ca2+]i was investigated in madin-darby canine kidney cells (mdck) by the fluorescent probes bcecf-am and fluo-4/am, respectively. the phi recovery rate was examined following the intracellular acidification after an nh4cl pulse, in presence of zero na+ plus schering 28080, which is a specific inhibitor of h+/k+-atpase.
Results:
Ang ii (10-12, 10-9 or 10-7 mol/l) increased the rate of phi recovery and [ca2+]i in a dose-dependent manner. anp (10-6 mol/l) or dimethyl-bapta/am (5 x 10-5 mol/l, an intracellular calcium chelator) did not affect the phi recovery but decreased [ca2+]i and blocked the stimulatory effect of ang ii on the phi recovery.
Conclusions:
The results suggest that the increase of [ca2+]i regulates the dose-dependent stimulatory effect of ang ii on h+-atpase. anp or dimethyl-bapta/am, by impairing the path causing the increase in [ca2+]i, blocks this stimulatory effect of ang ii.