1. The effect of PCO2 upon the discharge response to changes in P02 (between ca 450 and 30 mmHg) was observed in adult (> 5 weeks old) and neonatal (5-7 days old) rat carotid body chemoreceptors using an in vitro, superfused preparation.2. In both adult and neonatal rats, regression analysis revealed that increasing Pco2 was without effect upon the shape of the P02-response curves (P > 0 30), but did cause an upward shift in the position of the curves, as indicated by a significant increase in the baseline chemoreceptor discharge during hyperoxia (0 22 + 0 02% maximum discharge per mmHg PC02, P< 0001, and 0-25 + 007% maximum discharge per mmHg PCo2' P < 0 005, respectively). However, whilst increasing Pco2 caused a significant rightward shift of the response curves in adults (0 75 + 0-23 mmHg P02 per mmHg PC02; P < 0 005), it was without effect in neonates (Ofi21 + 0 fi22 mmHg Po2 per mmHg Pco2; P > 0 200). Thus increasing levels of hypoxia increased CO2 chemosensitivity in adult but not in neonatal rats as shown by multiple regression analysis of the C02-response curves which revealed a significant interaction between Pco2 and P02 for adult (P < 0 010) but not for neonatal (P> 0 150) rats. 3. We suggest that the previously reported maturation of peripheral chemoreceptor hypoxic sensitivity (resetting) may be due to the postnatal emergence of a significant degree of interaction between Pco, and Po0 at the level afferent innervation.

Ca2+-ATPase of the sarcoplasmic reticulum was localized in cryostat sections from three different adult canine skeletal muscles (gracilis, extensor carpi radialis, and superficial digitalis flexor) by immunofluorescence labeling with monoclonal antibodies to the Ca2+-ATPase. Type I (slow) myofibers were strongly labeled for the Ca2+-ATPase with a monoclonal antibody (I1 DS) to the Ca2+-ATPase of canine cardiac sarcoplasmic reticulum; the type I1 (fast) myofibers were labeled at the level of the background with monoclonal antibody I1 DS. By contrast, type I1 (fast) myofibers were strongly labeled for Ca2+-ATPase of rabbit skeletal sarcoplasmic reticulum. The subcellular distribution of the immunolabeling in type I (slow) myofibers with monoclonal antibody I1 DS corresponded to that of the sarcoplasmic reticulum as previously determined by electron microscopy. The structuraI similarity between the canine cardiac Ca2+-ATPase present in the sarcoplasmic reticulum of the canine slow skeletal muscle fibers was demonstrated by immunoblotting . Monoclonal antibody (I1 DS) to the cardiac Ca2+-ATPase binds to only one protein band present in the extract from either cardiac or type I (slow) skeletal muscle tissue. By contrast, monoclonal antibody (I1 H11) to the skeletal type I1 (fast) Ca2+-ATPase binds only one protein band in the extract from type I1 (fast) skeletal muscle tissue. These immunopositive proteins coelectrophoresed with the Ca2+-ATPase of the canine cardiac sarcoplasmic reticulum and showed an apparent M, of 115,000. It is concluded that the Ca2+-ATPase of cardiac and type I (slow) skeletal sarcoplasmic reticulum have at least one epitope in common, which is not present on the Ca2+-ATPase of sarcoplasmic reticulum in type I1 (fast) skeletal myofibers. It is possible that this site is related to the assumed necessity of the Ca2+-ATPase of the sarcoplasmic reticulum in cardiac and type I (slow) skeletal myofibers to interact with phosphorylated phospholamban and thereby enhance the accumulation of Ca2+ in the lumen of the sarcoplasmic reticulum following 6 -adrenergic stimulation.

Whole‐cell patch‐clamp recordings were used to investigate possible age‐related changes in K+ currents of type I carotid body cells isolated from the rat. K+ current density increased with age, as measured in cells isolated from 4‐day‐old, 10‐day‐old and adult rats (≥ 5 weeks old). The proportion of current reversibly inhibited by high [Mg2+] (6 mm), low [Ca2+] (0.1 mm) solutions, indicative of the proportion of current attributable to activation of Ca2+‐sensitive K+ (KCa) channels, was significantly smaller in cells of 4‐day‐old rats compared with 10‐dayold rats, despite inward Ca2+ current densities being similar in these two age groups. Inhibition of K+ currents by high [Mg2+], low [Ca2+] solutions was similar in 10‐day‐old and adult type I cells. Hypoxia (PO2, 16–23 mmHg) caused reversible reductions in type I cells from rats of all age groups. However, reductions seen in cells of 4‐day‐old rats were significantly smaller than those seen in cells of 10‐day‐olds and adults. The degree of hypoxic inhibition in these latter two groups was not significantly different. In the presence of high [Mg2+], low [Ca2+] solutions, hypoxia (PO2, 16–23 mmHg) was without significant effect on residual K+ currents in cells from all age groups. These observations indicate that K+ current density increases with postnatal age in the rat. Between days 4 and 10, there appears to be a predominant enhancement of KCa channels, and over the same age range hypoxic sensitivity of K+ currents increases. Our findings demonstrate that this latter observation arises because hypoxia selectively inhibits KCa channels in cells at all ages studied. These results suggest an important role for KCa channels in postnatal maturation of hypoxic chemoreception in the rat carotid body.

1. The effect of chronic hypoxaemia upon in vitro carotid body chemosensitivity was observed in eight rats > 5 weeks of age born and reared in 12 % oxygen. Comparisons were made with eight age-matched normoxic rats. 2. Single exponential functions with offset were fitted to the normalized (percentage of maximum) discharge responses to ramp decreases in Po2 at three steady levels of PC02. C02 sensitivity was derived from these functions. 3. Increasing hypercapnia increased the horizontal asymptote of the exponential functions in the normoxic (0-15 + 0 03 % discharge per mmHg Pco2; P < 0 001) and chronically hypoxic (0 13 + 0 04% discharge per mmHg Pco2; P < 0 005) animals but was without effect upon the rate constants in both groups (-0 04 + 0 18 mmHg Po2 per mmHg PC02, P > 0 50 and 063 + 048 mmHg P02 per mmHg Pco2, P > 0-20, respectively). Rate constants were greater in the chronically hypoxic animals (P < 0 05) compared with the normoxic animals.4. CO2 chemosensitivity increased with decreasing Po2 in normoxic (P < 005) but not in chronically hypoxic (P > 0 50) rats. 5. Our results show that chronic hypoxaemia from birth attenuates the maturation of C02-02 interaction at the carotid body.

Nearly one in five Mexican American children residing in California's San Joaquin Valley (the Valley) in 2007 had an asthma attack at some point in their life. Numerous epidemiological studies have suggested that compared with other ethnic groups and Latino subgroups residing in the United States, Mexican origin children have the lowest rates of pediatric asthma. Ethnographic research conducted in central California, however, suggests otherwise. Known for its agricultural produce, extreme poverty, and poor air quality, the Valley is a magnet for the Mexican immigrant farm worker population. We conducted an exploratory ethnographic study to examine health disparities, social suffering, and childhood asthma in the Valley. Many Valley residents believe that their children's health concerns are being ignored. Open-ended interviews uncovered a largely rural community suffering not only from the effects of childhood asthma but the inability to have their experiences taken seriously.