Stimulation of myocardial Na+-independent Cl-HCO3- exchanger by angiotensin II is mediated by endogenous endothelin

Maria C. Camilión De Hurtado, Bernardo V. Alvarez, Irene L. Ennis, Horacio E. Cingolani

Research output: Contribution to journalArticlepeer-review

Abstract

Experiments were performed in isolated cat papillary muscles loaded with the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein in the esterified form to study the effect of endothelin-1 (ET-1) on the activity of the Na+-independent Cl-HCO3- exchanger. Exposure to ET-1 (10 nmol/L) raised pH(i) by 0.13±0.03 U (P<0.05) in papillary muscles superfused with nominally HCO3--free solution, whereas no significant change was detected under CO2/HCO3- buffered medium. However, if ET-1 was applied to muscles pretreated with the anion exchanger inhibitor 4-acetamido-4'-isothiocyanato- stilbene-2,2'-disulfonic acid, pH(i) increased by 0.09±0.02 U (P<0.05) in the presence of CO2/HCO3- buffer. The rate of phi recovery from trimethylamine hydrochloride-induced intracellular alkaline load was enhanced so that net HCO3 efflux increased about three times in the presence of ET-1 (2.74±0.25 versus 9.66±1.29 mmol·L-1·min-1 at pH(i) 7.55, P<0.05). This effect was canceled by previous exposure to either 50 nmol/L PD 142,893 (nonselective endothelin receptor blocker) or 300 nmol/L BQ 123 (selective blocker of ET(A) receptors). BQ 123 also abolished angiotensin II-induced activation of the Na+ independent Cl-HCO3- exchanger. These results show that ET-1 increases the activity of the Na+-independent Cl-HCO3- exchanger in cardiac tissue through the ET(A) receptors. Furthermore, our data suggest that the previously described angiotensin II-induced stimulation of the anion exchanger activity is mediated by endogenous ET-1.

Original languageEnglish (US)
Pages (from-to)622-627
Number of pages6
JournalCirculation research
Volume86
Issue number6
DOIs
StatePublished - Mar 31 2000

Keywords

  • Angiotensin II
  • Anion exchanger
  • Endothelin-1
  • Na-H exchanger
  • Receptors, ET(A)

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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