Ca2+-dependence of endothelin-1 induced contraction of rat tail artery

Huang, Xiao; Takayanagi, Issei; Kurata, Ryuichi; Hisayama, Tetsuhiro

doi:10.1016/0306-3623(91)90471-h

Cited by 4 publications

(1 citation statement)

References 12 publications

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“…Our data also indicate that the Ang II‐mediated response is mainly dependent on intracellular Ca 2+ release whereas that of ET‐1 is primarily dependent on extracellular Ca 2+ entry. Our results are consistent with those reported by others ( Huang et al ., 1991 ; Morel et al ., 1996 ). Furthermore, Ang II evokes an additive contraction on top of the maximal response of the rat tail artery to ET‐1, supporting our conclusion that Ang II and ET‐1 utilize distinct signalling pathways.…”

Section: Discussionsupporting

confidence: 94%

Lack of involvement of endothelin‐1 in angiotensin II‐induced contraction of the isolated rat tail artery

Jiang

Triggle

2000

British J Pharmacology

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1 The contribution of endothelin-1 (ET-1) to angiotensin II (Ang II)-mediated contraction of the isolated rat tail artery was assessed with measurements of tension, and cytosolic calcium ([Ca 2+ ] i ). The distribution of the AT 1 receptor was studied with RT ± PCR and immunohistochemistry. 2 Ang II induced an endothelium-independent contraction (pEC 50 7.95+0.06 and E max : 0.46 g+0.05 with endothelium vs 7.81+0.02 and 0.41 g+0.07 without endothelium; P40.05). Ang II (0.003 ± 0.3 mM)-induced a non-sustained contraction of endothelium-intact preparations which was not antagonized by BQ-123 (1 mM), but was inhibited by losartan (10 nM). In addition, the maximal contraction induced by ET-1 (0.1 mM) could be further increased by the addition of 0.1 mM Ang II. 4 Ang II-induced contraction was insensitive to inhibition by nifedipine (0.1 mM), an antagonist of L-type voltage-gated Ca 2+ channels, and SK&F96365 (10 mM), which blocks non-selective cation channels, whereas that to ET-1 was inhibited by SK&F69365. 5 RT ± PCR data indicate the expression of AT 1A and AT 1B on both VSMCs and endothelial cells, but immunohistochemical evidence illustrates that the AT 1 is located primarily on VSMCs. 6 These results indicate that endothelium-derived ET-1 is not involved in the Ang II-mediated vasoconstriction of the rat tail artery and that Ang II-and ET-1-mediated VSM contractions utilize distinct pathways.

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Section: Discussionsupporting

confidence: 94%