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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Effects of angiotensin metabolites in the coronary vascular bed of the spontaneously hypertensive rat: loss of angiotensin II type 2 receptor-mediated vasodilation.
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Effects of angiotensin metabolites in the coronary vascular bed of the spontaneously hypertensive rat: loss of angiotensin II type 2 receptor-mediated vasodilation.

机译：自发性高血压大鼠冠状血管床中血管紧张素代谢产物的影响：血管紧张素II 2型受体介导的血管舒张功能丧失。

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摘要

Because angiotensin (Ang) metabolites mediate functions independent of Ang II, we investigated their effects on coronary flow in spontaneously hypertensive rats (SHRs). Results were compared with those in the iliac artery and abdominal aorta and the coronary circulation of the Wistar rat. Ang II, III, and IV decreased coronary flow in SHRs and Wistar rats, with Ang III and IV being approximately 10 and approximately 1000 times less potent than Ang II. Ang-(1-7) decreased coronary flow at concentrations >1 micromol/L in SHRs. The Ang II type 1 receptor antagonist irbesartan blocked the effects of Ang II, III, and IV, whereas the Ang II type 2 receptor antagonist PD123319 blocked the effects of Ang-(1-7). The maximal Ang II- and III-induced decreases in coronary flow in SHRs were twice as large as those in Wistar rats. PD123319 enhanced the constrictor effects of Ang II and III in Wistar rats so that, in the presence of this drug, their effects were comparable to those in SHRs. In contrast, PD123319 did not alter the Ang II- and III-induced responses in SHRs and blocked the constrictor effect of Ang II in iliac arteries. Ang II type 2 receptor-mediated relaxation did not occur in iliac arteries and abdominal aortas, and the constrictor effects of Ang metabolites in these vessels were identical in Wistar rats and SHRs. In conclusion, coronary constriction induced by Ang II, Ang III, and Ang-(1-7) is enhanced in SHRs as compared with Wistar rats. This is attributable to the absence of counterregulatory Ang II type 2 receptor-mediated relaxation and/or a change of the Ang II type 2 receptor phenotype from relaxant to constrictor.
机译：因为血管紧张素（Ang）代谢产物介导的功能独立于Ang II，所以我们调查了它们对自发性高血压大鼠（SHRs）冠状动脉血流的影响。将结果与Wistar大鼠的artery动脉和腹主动脉以及冠状动脉循环的结果进行比较。 Ang II，III和IV降低了SHR和Wistar大鼠的冠状动脉血流量，Ang III和IV的效力比Ang II低约10倍和约1000倍。 Ang-（1-7）在SHRs中浓度> 1 micromol / L时会降低冠脉血流。 Ang II 1型受体拮抗剂厄贝沙坦阻断了Ang II，III和IV的作用，而Ang II 2型受体拮抗剂PD123319阻断了Ang-（1-7）的作用。 SHRs中最大的Ang II和III诱导的冠状动脉血流减少量是Wistar大鼠的两倍。 PD123319增强了Ang II和III对Wistar大鼠的收缩作用，因此，在存在这种药物的情况下，其作用与SHRs相当。相反，PD123319并未改变SHR中Ang II和III诱导的反应，并阻止了Ang II对动脉的收缩作用。在动脉和腹主动脉中未发生Ang II 2型受体介导的舒张，Wistar大鼠和SHRs在这些血管中Ang代谢产物的收缩作用相同。总之，与Wistar大鼠相比，SHRs中由Ang II，Ang III和Ang-（1-7）诱导的冠状动脉收缩得到增强。这归因于不存在抗调节的Ang II 2型受体介导的松弛和/或Ang II 2型受体表型从松弛剂变为收缩剂的变化。

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