Angiotensin II attenuates vascular contractility in the rabbit mesenteric artery.
We observed the effects of angiotensin II (AII) on the contractile response and the Ca2+ transient induced by high K+ solution in the rabbit mesenteric artery. In the control condition, the repeated application of high K+ solution with 90 min interval induced a gradually increasing contraction, which was accompanied with a significant elevation of the intracellular calcium concentration ([Ca2+]i). Treatment of the tissue with AII for one to two hours abolished the incremental response of the contraction. The change in [Ca2+]i induced by high K+ solution, however, was not significantly different with and without treatment with AII. Pretreatment of the tissue with actinomycin D abolished the inhibitory action of AII on the incremental contraction, indicating the involvement of a transcriptional process. These results indicate that AII impairs vascular contractility through the modulation of Ca(2+)-sensitivity of the contractile machinery.
Oike
M
M
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Takahashi
N
N
Ito
Y
Y
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects*; D007700:Kinetics; D008638:Mesenteric Arteries / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D013997:Time Factors
D000804:Angiotensin II; D011188:Potassium; D002118:Calcium