Differences in the role of Na+/K+-ATPase during alpha 1-adrenergic events in rat and rabbit aorta.

Transport activity of the Na+/K+-ATPase was studied in rat and rabbit aorta under basal and agonist-stimulated conditions. Basal ouabain-sensitive 86Rb+ uptake was 2.9-fold higher in rat tissues as compared to rabbit tissues. This higher uptake in the rat was associated with a greater sensitivity to the Na+/H+ exchange inhibitor amiloride. Stimulation of alpha 1-adrenergic receptors by norepinephrine (NE) or phenylephrine (PE) resulted in an increase in ouabain-sensitive 86Rb+ uptake, whose temporal pattern differed between arteries of the two species. In rat aorta the increase was maximal during the first 2 min of agonist exposure reaching approximately a 50% higher rate of uptake than controls while rabbit aorta exhibited a steady rise in 86Rb+ uptake. Removal of extracellular Ca2+ by EGTA (1 mM) for 10 min resulted in an activation of Na+/K+-ATPase-related 86Rb+ uptake after which PE was still capable of causing a further increase, suggesting that Ca2+ influx is not responsible for the receptor-induced stimulation. Removal of extracellular Na+ reduced the PE-induced stimulation, while amiloride did not block the agonist effect. To characterize the role of the Na+/K+-ATPase during contractile events, receptor-induced 45Ca2+ uptake, 45Ca2+ release and contraction were compared in rat and rabbit aorta following Na+/K+-ATPase inhibition. Rat responses to PE were readily inhibited by ouabain or K+-free conditions, while rabbit responses were relatively resistant. 45Ca2+ extrusion and relaxation following alpha 1-adrenergic receptor stimulation were both highly dependent on activity of the Na+/K+-ATPase in rat aorta. These species' differences in Na+/K+-ATPase transport activity and its role in the regulation of contractility illustrate an example of heterogeneity in the ionic control of arterial tone.