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同源血管紧张素II对一种软骨鱼离体动脉环制剂的直接血管收缩作用。

Direct vasoconstrictor action of homologous angiotensin II on isolated arterial ring preparations in an elasmobranch fish.

作者信息

Hamano K, Tierney M L, Ashida K, Takei Y, Hazon N

机构信息

National Research Institute of Fisheries Science, Yokohama, Japan.

出版信息

J Endocrinol. 1998 Sep;158(3):419-23. doi: 10.1677/joe.0.1580419.

DOI:10.1677/joe.0.1580419
PMID:9846171
Abstract

Arterial rings were prepared from the branchial artery, coeliac artery and ventral aorta of the Japanese dogfish Triakis scyllia and used to determine arterial contraction in a myograph. Noradrenaline caused a dose-dependent contraction (10(-9)-3 x 10(-6) M) that was completely inhibited by pre-treatment with 10(-7) M phentolamine. Homologous dogfish angiotensin II (ANG II) ([Asn1, Pro3, Ile5]-ANG II) also caused dose-dependent contraction (10(-9)-3 x 10(-6) M), but phentolamine had no effect on this response. Administration of dogfish angiotensin I (ANG-I) ([Asn1, Pro3, Ile5, Gln9]-ANG I) resulted in a contraction similar to that produced by ANG II and the effect could be blocked with 10(-7) M captopril. The mammalian ANG II receptor antagonists [Sar1, Ile8]-ANG II and [Sar1, Ala8]-ANG II caused dose-dependent contractions of coeliac artery rings, but were less potent than homologous ANG I and ANG II. These results show that the contractile effect of [Asn1, Pro3, Ile5]-ANG II is not mediated by the alpha-adrenergic system and contractions of arterial rings by noradrenaline and elasmobranch ANG II are mediated by separate vascular receptors. The elasmobranch ANG II vascular receptor may have co-evolved with the unusual structure of this peptide.

摘要

从日本角鲨(Triakis scyllia)的鳃动脉、腹腔动脉和腹主动脉制备动脉环,并用于在肌动描记器中测定动脉收缩情况。去甲肾上腺素引起剂量依赖性收缩(10(-9)-3×10(-6)M),预先用10(-7)M酚妥拉明处理可完全抑制该收缩。同源角鲨血管紧张素II(ANG II)([天冬酰胺1,脯氨酸3,异亮氨酸5]-ANG II)也引起剂量依赖性收缩(10(-9)-3×10(-6)M),但酚妥拉明对该反应无影响。给予角鲨血管紧张素I(ANG-I)([天冬酰胺1,脯氨酸3,异亮氨酸5,谷氨酰胺9]-ANG I)导致的收缩与ANG II产生的收缩相似,且该效应可被10(-7)M卡托普利阻断。哺乳动物ANG II受体拮抗剂[肌氨酸1,异亮氨酸8]-ANG II和[肌氨酸1,丙氨酸8]-ANG II引起腹腔动脉环的剂量依赖性收缩,但效力低于同源ANG I和ANG II。这些结果表明,[天冬酰胺1,脯氨酸3,异亮氨酸5]-ANG II的收缩作用不是由α-肾上腺素能系统介导的,去甲肾上腺素和板鳃亚纲动物ANG II引起的动脉环收缩是由不同的血管受体介导的。板鳃亚纲动物ANG II血管受体可能与其该肽的特殊结构共同进化。

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