Segments of the ventral tail artery from DCA-hypertensive and normotensive rats were artificially perfused at pressures from 60 to 120 mm Hg. Contraction of the segments was induced by the addition of norepinephrine to the perfusate or by increasing the K+ concentration of the perfusate. Contraction was abolished by removing Ca++ from the perfusate and re-established by addingCa++ to the Ca++-free perfusate.
The experiments demonstrate hyperresponsiveness of the hypertensive artery in three ways: first, the hypertensive artery performed more work than the normotensive artery; second, contraction in the hypertensive artery was more difficult to abolish during zero Ca++ perfusion; and third, less Ca++ was required to re-establish the abolished contraction in the hypertensive artery.
When the artificially perfused artery segments were analyzed for cations, the hypertensive arteries were found to contain increased amounts of Na+, K+, Mg++, and Ca++. After zero Ca++-Krebs perfusion, the hypertensive and normotensive arteries contained similar amounts of Ca++ and Mg++, indicating that more Ca++ was removed from the hypertensive artery.
The results suggest that hyperresponsiveness may be due to an increased efficiency in either Ca++ utilization during excitation coupling or in the contractile mechanism itself.
- © 1966 American Heart Association, Inc.