Angiotensin II Activates Na+-Independent Cl--HCO3- Exchange in Ventricular Myocardium

The effect of angiotensin II (Ang II) on the activity of the cardiac Na Cl3 exchanger (anionic exchanger [AE]) was explored in cat papillary muscles. pHi was measured by epifluorescence with BCECF-AM. Ang II (500 nmol/L) induced a 5-(N-ethyl-N-isopropyl)amiloride-sensitive increase in pHi in the abs...

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Bibliographic Details
Published in:Circulation research 1998-03, Vol.82 (4), p.473-481
Main Authors: de Hurtado, Maria C. Camilion, Alvarez, Bernardo V, Perez, Nestor G, Ennis, Irene L, Cingolani, Horacio E
Format: Article
Language:English
Subjects:
Alkaloids
Amiloride - analogs & derivatives
Amiloride - pharmacology
Angiotensin II - physiology
Angiotensin Receptor Antagonists
Animals
Antiporters - metabolism
Benzophenanthridines
Bicarbonates - metabolism
Biological and medical sciences
Cats
Chloride-Bicarbonate Antiporters
Chlorides - metabolism
Enzyme Inhibitors - pharmacology
Fundamental and applied biological sciences. Psychology
Heart
Heart Ventricles - metabolism
Hydrogen-Ion Concentration
In Vitro Techniques
Losartan - pharmacology
Myocardium - metabolism
Phenanthridines - pharmacology
Protein Kinase C - antagonists & inhibitors
Receptor, Angiotensin, Type 1
Receptor, Angiotensin, Type 2
Signal Transduction
Sodium - metabolism
Sodium-Hydrogen Exchangers - antagonists & inhibitors
Vertebrates: cardiovascular system
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Summary:The effect of angiotensin II (Ang II) on the activity of the cardiac Na Cl3 exchanger (anionic exchanger [AE]) was explored in cat papillary muscles. pHi was measured by epifluorescence with BCECF-AM. Ang II (500 nmol/L) induced a 5-(N-ethyl-N-isopropyl)amiloride-sensitive increase in pHi in the absence of external HCO3 (HEPES buffer), consistent with its stimulatory action on Na exchange (NHE). This alkalinizing effect was not detected in the presence of a CO2-HCO3 buffer (pH (i) 7.07 +/- 0.02 and 7.08 +/- 0.02 before and after Ang II, respectively; n=17). Moreover, in Na HCO3 medium, in which neither NHE nor Na3 cotransport are acting, Ang II decreased pHi, and this effect was canceled by previous treatment with SITS. These findings suggested that the Ang II-induced activation of NHE was masked, in the presence of the physiological buffer, by a HCO3 acidifying mechanism, probably the AE. This hypothesis was confirmed on papillary muscles bathed with HCO3 buffer that were first exposed to 1 [micro sign]mol/L S20787, a specific inhibitor of AE activity in cardiac tissue, and then to 500 nmol/L Ang II (n=4). Under this condition, Ang II increased pHi from 7.05 +/- 0.05 to 7.22 +/- 0.05 (P
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.82.4.473