Intracellular pH regulation of normal and hypertrophic rat myocardium.
The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.
D000136:Acid-Base Equilibrium; D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications; D001639:Bicarbonates / Q000378:metabolism; D002021:Buffers; D002245:Carbon Dioxide; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats
D001639:Bicarbonates; D002021:Buffers; D002245:Carbon Dioxide