Inhibition of Erythrocyte Na,K-ATPase Activity During Anticipatory Hypoventilation in Micropigs
Previous studies with micropigs showed that conditioned suppression of respiration preceding the onset of an avoidance task was associated with increased pCO 2, decreased plasma pH, decreased hematocrit, and increased blood pressure with no change in heart rate. Voluntary hypoventilation by humans,...
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Veröffentlicht in: | American journal of hypertension 1996-11, Vol.9 (11), p.1126-1131 |
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Zusammenfassung: | Previous studies with micropigs showed that conditioned suppression of respiration preceding the onset of an avoidance task was associated with increased pCO
2, decreased plasma pH, decreased hematocrit, and increased blood pressure with no change in heart rate. Voluntary hypoventilation by humans, which evoked similar effects, was found to elicit increases in plasma endogenous digitalis-like factors (EDLF) and decreases in erythrocyte Na,K-ATPase. The present study investigated plasma EDLF and Na,K-ATpase activity in micropigs preceding and during avoidance sessions. Compared with levels in a controlled environment, 1 h of quiet waiting for the onset of a 30-min avoidance task was associated with hypoventilation, acidification of the plasma, and a decrease in hematocrit with progressive increases in plasma EDLF, and decreases in erythrocyte Na,K-ATPase activity (1.67 ± 0.35
v 2.73 ± 0.24 μmol P
i/mL er/h). Systolic blood pressure increased (126.5 ± 5.7
v 121.7 ± 4.2 mm Hg) during preavoidance periods, with no changes in heart rate (89.5 ± 3.9
v 89.4 ± 4.0 beats/min). During the avoidance sessions, plasma EDLF, systolic blood pressure (126.7 ± 4.5 mm Hg), and heart rate (107.3 ± 4.8 beats/min) were elevated above the first 10 min of preavoidance, whereas Na,K-ATPase activity returned toward control values (2.46 ± 0.83 μmol P
i/mL er/h). These findings are consistent with the view that elevation of blood pressure during behaviorally induced hypoventilation in micropigs is mediated in part by inhibition of Na,K-ATPase by increases in plasma EDLF due to expanded plasma volume. Am J Hypertens 1996;9:1126–1131 |
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ISSN: | 0895-7061 1879-1905 1941-7225 |
DOI: | 10.1016/0895-7061(96)00194-X |