1. We have previously shown that the cytosolic acid concentration changes in skeletal muscle during contraction in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats in vivo. We have now found that this change was unaffected by 20% inhaled CO2 or by 4,4′-di-isothiocyanostilbene-2,2′-disulphonate. This is evidence that HCO3− exchange in vivo is not important in the control of cytosolic acid concentration during skeletal muscle contraction in either spontaneously hypertensive or Wistar-Kyoto rats.
2. We have also previously shown that the difference in cytosolic acid response during contraction between spontaneously hypertensive and Wistar-Kyoto rats is due to increased Na+/H+ antiporter activity in the spontaneously hypertensive rats. Our current findings suggest that this increase in Na+/H+ antiporter activity is more likely to be due to a change in the Km of the antiporter than to a change in the Vmax. We estimate that the Km of the antiporter changes in hypertension from pH 7.16 to 7.33.
3. We did not find any differences between adult spontaneously hypertensive and Wistar-Kyoto rats with regard to resting intracellular and extracellular pH and resting intracellular and extracellular HCO3− concentrations. In addition, we did not find any evidence of a difference in skeletal muscle HCO3−/Cl− exchange between adult spontaneously hypertensive and Wistar-Kyoto rats.
4. At rest, skeletal muscles of the spontaneously hypertensive and Wistar-Kyoto rats have the same lactate production, HCO3−/Cl− exchange and arterial partial pressure of CO2. In addition, we can also calculate that at a resting intracellular pH of 7.05 in the spontaneously hypertensive rats, the antiporter is 66% saturated. The corresponding value in the Wistar-Kyoto rats (resting intracellular pH 7.04) is 57%. This explains the lack of difference in resting intracellular pH between the two strains of rat and suggests that at rest differences in Na+/H+ antiporter activity due to a shift in Km of the antiporter are too small to result in a difference in resting pH.
5. Furthermore, Na+/H+ antiporter activity around pH 7.0 was unable to prevent the acidosis caused by CO2 loading. Thus resting pH in skeletal muscle in vivo is determined largely by the HCO3− system and in this regard skeletal muscle is similar to vascular smooth muscle.