Abstract
This study examined whether alterations in intracellular or extracellular Ca 2+ mobilization were related to differences in caffeine and phenylephrine (PHE)-induced contractions between two-kidney, one-clip hypertensive (2K-1C) and normotensive (2K) rat aortas. After depletion and reloading of intracellular Ca 2+ stores, caffeine and PHE-induced contractions in Ca 2+-free solution were increased in 2K-1C. Thapsigargin reduced the contraction to caffeine in 2K-1C and 2K with similar sensitivity. PHE-induced contraction in 1.6-mM Ca 2+ solution was decreased in 2K-1C, and nifedipine was less effective in lowering this response. The responsiveness to extracellular Ca 2+ was decreased in 2K-1C hypertensive rat aortas. Our results indicate an increased intracellular Ca 2+ stores that are not related to alteration in Ca 2+-ATPase function and a lower contribution of L-type channels to the contraction of 2K-1C aortas.
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