INHIBITION OF ERYTHROCYTE NA,K-ATPASE ACTIVITY DURING ANTICIPATORY HYPOVENTILATION IN MICROPIGS

Citation
Ov. Fedorova et al., INHIBITION OF ERYTHROCYTE NA,K-ATPASE ACTIVITY DURING ANTICIPATORY HYPOVENTILATION IN MICROPIGS, American journal of hypertension, 9(11), 1996, pp. 1126-1131
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
08957061
Volume
9
Issue
11
Year of publication
1996
Pages
1126 - 1131
Database
ISI
SICI code
0895-7061(1996)9:11<1126:IOENAD>2.0.ZU;2-9
Abstract
Previous studies with micropigs showed that conditioned suppression of respiration preceding the onset of an avoidance task was associated w ith increased pCO(2), decreased plasma pH, decreased hematocrit, and i ncreased blood pressure with no change in heart rate. Voluntary hypove ntilation by humans, which evoked similar effects, was found to elicit increases in plasma endogenous digitalis-like factors (EDLF) and decr eases in erythrocyte Na,K-ATPase. The present study investigated plasm a EDLF and Na,K-ATPase activity in micropigs preceding and during avoi dance sessions. Compared with levels in a controlled environment, Ih o f quiet waiting for the onset of a 30-min avoidance task was associate d with hypoventilation, acidification of the plasma, and a decrease in hematocrit with progressive increases in plasma EDLF, and decreases i n erythrocyte Na,K-ATPase activity (1.67 +/- 0.35 v 2.73 +/- 0.24 mu m ol P-i/mL er/h). Systolic blood pressure increased (126.5 +/- 5.7 v 12 1.7 +/- 4.2 mm Hg) during preavoidance periods, with no changes in hea rt 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 mu mol P-i/mL er/h). These Endings are c onsistent with the view that elevation of blood pressure during behavi orally induced hypoventilation in micropigs is mediated in part by inh ibition of Na,K-ATPase by increases in plasma EDLF due to expanded pla sma volume.