This study was designed to establish the relationship between urinary pCO2 and systemic blood pCO2 during acute hypercapnia and to investigate the significance of this relationship to collecting duct hydrogen ion (H+) secretion when the urine is acid and when it is highly alkaline. In rats excreting a highly alkaline urine, an acute increase in blood pCO2 (from 42±0.8 to 87±0.8 mmHg) resulted in a significant fall in urine minus blood (U-B) pCO2 (from 31.±2.0 to 16±4.2 mmHg, P<0.005), a finding which could be interpreted to indicate inhibition of collecting duct H+ secretion by hypercapnia. The urinary pCO2 of rats with hypercapnia, unlike that of normocapnic controls, was significantly lower than that of blood when the urine was acid (58±6.3 and 86±1.7 mmHg, P< 0.001) and when it was alkalinized in the face of accelerated carbonic acid dehydration by infusion of carbonic anhydrate (78±2.7 and 87±1.8 mmHg, P<0.02). The finding of a urinary pCO2 lower than systemic blood pCO2 during hypercapnia suggested that the urine pCO2 prevailing before bicarbonate loading should be known and the blood pCO2 kept constant to evaluate collecting duct H+ secretion using the urinary pCO2 technique. In experiments performed under these conditions, sodium bicarbonate infusion resulted in an increment in urinary pCO2 (i.e., a ΔpCO2) which was comparable in hypercapnic and normocapnic rats (40±7.2 and 42±4.6 mmHg, respectively) that were alkalemic (blood pH 7.53±0.02 and 7.69±0.01, respectively). The U-B pCO2, however, was again lower in hypercapnic than in normocapnic rats (15±4.0 and 39±2.5 mmHg, respectively, P<0.001). In hypercapnic rats in which blood pH during bicarbonate infusion was not allowed to become alkalemic (7.38±0.01), the ΔpCO2 was higher than that of normocapnic rats which were alkalemic (70±5.6 and 42±4.6 mmHg, respectively, P<0.005) while the U-B pCO2 was about the same (39±3.7 and 39±2.5 mmHg). We further examined urine pCO2 generation by measuring the difference between the urine pCO2 of a highly alkaline urine not containing carbonic anhydrase and that of an equally alkaline urine containing this enzyme. Carbonic anhydrase infusion to hypercapnic rats that were not alkalemic resulted in a fall in urine pCO2 (from 122±5.7 to 77±2.2 mmHg) which was greater (P<0.02) than seen in alkalemic normocapnic controls (from 73±1.9 to 43±1.3 mmHg) with a comparable urine bicarbonate concentration and urine nonbicarbonate buffer capacity. CO2 generation, therefore, from collecting duct H+ secretion and titration of bicarbonate, was higher in hypercapnic rats than in normocapnic controls. We conclude that in rats with acute hypercapnia, the U-B pCO2 achieved during bicarbonate loading greatly underestimates collecting duct H+ secretion because it is artificially influenced by systemic blood pCO2. The ΔpCO2 is a better qualitative index of collecting duct H+ secretion than the U-B pCO2, because it is not artificially influenced by systemic blood pCO2 and it takes into account the urine pCO2 prevailing before bicarbonate loading.
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