TY - JOUR
T1 - Hyperactivity and altered mRNA isoform expression of the Cl-/HCO3- anion-exchanger in the hypertrophied myocardium
AU - Chiappe De Cingolani, Gladys
AU - Morgan, Patricio
AU - Mundiña-Weilenmann, Cecilia
AU - Casey, Joseph
AU - Fujinaga, Jocelyne
AU - Camilión De Hurtado, María
AU - Cingolani, Horacio
N1 - Funding Information:
This work was supported in part by funds from the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) PIP 4715/96, Argentina. P.M. was a recipient of a fellowship from Comisión de Investigaciones Científicas (Pcia de Bs. As) and Fundación Antorchas, Argentina (year 2000). G.Ch.deC., C.M.-W, M.C.deH. and H.C. are established investigators of CONICET. J.C. is a Scholar of the Alberta Heritage Foundation for Medical Research and Medical Research Council of Canada.
PY - 2001
Y1 - 2001
N2 - Objective: The aim was to examine the regulation of the cardiac Na+-independent Cl-/HCO3- exchanger (AE) mRNA isoform expression in association to the enhanced AE activity in the hypertrophied myocardium of spontaneously hypertensive rats (SHR). Methods: AE activity was determined by the initial rates of the pHi recovery from imposed intracellular alkalinization (forward mode of exchange) and the pHi rise induced by Cl- removal (reverse mode). Net HCO3- (JHCO3-) efflux and influx were respectively determined. AE mRNA isoforms were analyzed by Northern blot with specific probes to detect AE1, AE2 and AE3 mRNAs. Results: Initial JHCO3- efflux after imposed alkaline load (pHi≅7.5) was higher in SHR than in normotensive WKY rats (3.01±0.33, n=7, vs. 0.64±0.29 mM/min, n=5, P<0.05). JHCO3- influx induced by Cl- deprivation was also increased in SHR, 4.24±0.56 mM/min (n=10) versus 2.31±0.26 (n=10, P<0.05) in WKY. In arbitrary units, the 4.1-kb AE1 mRNA decreased in SHR (0.15±0.01, n=7) compared to WKY (0.29±0.06, n=7, P<0.05), whereas the 3.6-kb mRNA did not change. AE2 mRNAs were similarly expressed in WKY and SHR. Cardiac specific AE3 (cAE3) mRNA decreased in SHR, 1.10±0.16 arbitrary units (n=8) versus 1.79±0.24, (n=8, P<0.05) in WKY. Full length AE3 (flAE3) mRNA increased from 0.69±0.06 (WKY, n=8) to 1.25±0.19 arbitrary units in SHR (n=8, P<0.05). Conclusions: The increase in flAE3 mRNA expression in cardiac tissue from the SHR is an adaptive change of the hypertrophied myocardium that might be in connection with the increased activity of the AE.
AB - Objective: The aim was to examine the regulation of the cardiac Na+-independent Cl-/HCO3- exchanger (AE) mRNA isoform expression in association to the enhanced AE activity in the hypertrophied myocardium of spontaneously hypertensive rats (SHR). Methods: AE activity was determined by the initial rates of the pHi recovery from imposed intracellular alkalinization (forward mode of exchange) and the pHi rise induced by Cl- removal (reverse mode). Net HCO3- (JHCO3-) efflux and influx were respectively determined. AE mRNA isoforms were analyzed by Northern blot with specific probes to detect AE1, AE2 and AE3 mRNAs. Results: Initial JHCO3- efflux after imposed alkaline load (pHi≅7.5) was higher in SHR than in normotensive WKY rats (3.01±0.33, n=7, vs. 0.64±0.29 mM/min, n=5, P<0.05). JHCO3- influx induced by Cl- deprivation was also increased in SHR, 4.24±0.56 mM/min (n=10) versus 2.31±0.26 (n=10, P<0.05) in WKY. In arbitrary units, the 4.1-kb AE1 mRNA decreased in SHR (0.15±0.01, n=7) compared to WKY (0.29±0.06, n=7, P<0.05), whereas the 3.6-kb mRNA did not change. AE2 mRNAs were similarly expressed in WKY and SHR. Cardiac specific AE3 (cAE3) mRNA decreased in SHR, 1.10±0.16 arbitrary units (n=8) versus 1.79±0.24, (n=8, P<0.05) in WKY. Full length AE3 (flAE3) mRNA increased from 0.69±0.06 (WKY, n=8) to 1.25±0.19 arbitrary units in SHR (n=8, P<0.05). Conclusions: The increase in flAE3 mRNA expression in cardiac tissue from the SHR is an adaptive change of the hypertrophied myocardium that might be in connection with the increased activity of the AE.
KW - Gene expression
KW - Hypertension
KW - Hypertrophy
KW - Ion exchangers
KW - Membrane transport
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U2 - 10.1016/S0008-6363(01)00276-0
DO - 10.1016/S0008-6363(01)00276-0
M3 - Article
C2 - 11399249
AN - SCOPUS:0035021017
SN - 0008-6363
VL - 51
SP - 71
EP - 79
JO - Cardiovascular research
JF - Cardiovascular research
IS - 1
ER -