Physical and Functional Interaction of Carbonic Anhydrases and NBCe1 Na+/HCO3- Cotransporter in the Heart. The Metabolon Revisited.

ALVAREZ BV; AIELLO EA

Physiological Mini-Reviews

Argentine Physiological Society

Año: 2012 vol. 6 p. 26 - 36

1669-5402

To allow the control of their intracellular pH (pHi) and bicarbonate (HCO3) levels, cells express HCO3 transport proteins (NBC) that rapidly and selectively move HCO3 across the plasma membrane. In the heart electroneutral NBCn1 and electrogenic NBCe1 Na+/HCO3 cotransporters facilitate the transmembrane movement of HCO3  ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO2i) and bicarbonate (HCO3) levels, cells express HCO3 transport proteins (NBC) that rapidly and selectively move HCO3 across the plasma membrane. In the heart electroneutral NBCn1 and electrogenic NBCe1 Na+/HCO3 cotransporters facilitate the transmembrane movement of HCO3  ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO23 transport proteins (NBC) that rapidly and selectively move HCO3 across the plasma membrane. In the heart electroneutral NBCn1 and electrogenic NBCe1 Na+/HCO3 cotransporters facilitate the transmembrane movement of HCO3  ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO23 across the plasma membrane. In the heart electroneutral NBCn1 and electrogenic NBCe1 Na+/HCO3 cotransporters facilitate the transmembrane movement of HCO3  ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO2+/HCO3 cotransporters facilitate the transmembrane movement of HCO3  ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO2 ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO22 to HCO3, to form a transport metabolon, a weakly associated complex of sequential metabolic enzymes. NBCe1 physically/functionally interact with the isoforms II, IV, and IX of CA, to increase the HCO3 flux through cell membranes. NBCe1 and CAs interaction occurs in different cellular compartments in the heart muscle. Physiologically, the NBCe1/CA complex could contribute to the removal of H+ ions accumulated as the result of the contractile activity of the cardiac muscle cell, and this process may occur at the surface sarcolemma (CAII-NBCe1-CAIV complex) or at the ttubule (CAII-NBCe1-CAIX complex) of the cardiomyocyte. Pathologically, upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells.3, to form a transport metabolon, a weakly associated complex of sequential metabolic enzymes. NBCe1 physically/functionally interact with the isoforms II, IV, and IX of CA, to increase the HCO3 flux through cell membranes. NBCe1 and CAs interaction occurs in different cellular compartments in the heart muscle. Physiologically, the NBCe1/CA complex could contribute to the removal of H+ ions accumulated as the result of the contractile activity of the cardiac muscle cell, and this process may occur at the surface sarcolemma (CAII-NBCe1-CAIV complex) or at the ttubule (CAII-NBCe1-CAIX complex) of the cardiomyocyte. Pathologically, upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells.3 flux through cell membranes. NBCe1 and CAs interaction occurs in different cellular compartments in the heart muscle. Physiologically, the NBCe1/CA complex could contribute to the removal of H+ ions accumulated as the result of the contractile activity of the cardiac muscle cell, and this process may occur at the surface sarcolemma (CAII-NBCe1-CAIV complex) or at the ttubule (CAII-NBCe1-CAIX complex) of the cardiomyocyte. Pathologically, upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells.+ ions accumulated as the result of the contractile activity of the cardiac muscle cell, and this process may occur at the surface sarcolemma (CAII-NBCe1-CAIV complex) or at the ttubule (CAII-NBCe1-CAIX complex) of the cardiomyocyte. Pathologically, upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells.upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells.