Hicks P E, Medgett I C, Langer S Z
Hypertension. 1984 Mar-Apr;6(2 Pt 2):I12-8. doi: 10.1161/01.hyp.6.2_pt_2.i12.
In isolated perfused tail arteries of spontaneously hypertensive rats (SHR), the selective alpha 2-adrenergic receptor antagonist idazoxan ( RX781094 ) at low concentrations antagonized vasoconstrictor responses induced by norepinephrine (NE) and low frequency periarterial field stimulation. The vasoconstrictor responses to the selective alpha 2-adrenergic receptor agonist TL99 or to phenylephrine were also antagonized by low concentrations of idazoxan . In contrast, idazoxan did not antagonize responses induced by the alpha 1-adrenergic receptor agonists amidephrine or methoxamine in perfused tail arteries of SHR. The alpha 1-adrenergic receptor antagonist prazosin was very potent against methoxamine or phenylephrine and responses to periarterial field stimulation in SHR and Wistar-Kyoto (WKY) rat tail arteries, but only showed a modest selectivity for TL99 -induced responses in SHR arteries. The results support the contention that postjunctional alpha 2-adrenergic receptors can be demonstrated in arterial smooth muscle in vitro and are particularly evident in arteries from hypertensive animals. In SHR tail arteries, postsynaptic alpha 2-adrenergic receptors contribute to the vasoconstrictor responses to exogenous NE and may be activated by endogenously released NE.
在自发性高血压大鼠（SHR）的离体灌注尾动脉中，低浓度的选择性α2-肾上腺素能受体拮抗剂咪唑克生（RX781094）可拮抗去甲肾上腺素（NE）和低频动脉周围场刺激诱导的血管收缩反应。低浓度的咪唑克生还可拮抗对选择性α2-肾上腺素能受体激动剂TL99或去氧肾上腺素的血管收缩反应。相比之下，咪唑克生并不拮抗SHR灌注尾动脉中α1-肾上腺素能受体激动剂酰胺福林或甲氧明诱导的反应。α1-肾上腺素能受体拮抗剂哌唑嗪对SHR和Wistar-Kyoto（WKY）大鼠尾动脉中的甲氧明或去氧肾上腺素以及对动脉周围场刺激的反应非常有效，但对SHR动脉中TL99诱导的反应仅表现出适度的选择性。这些结果支持了这样的观点，即体外可在动脉平滑肌中证明节后α2-肾上腺素能受体，并且在高血压动物的动脉中尤为明显。在SHR尾动脉中，突触后α2-肾上腺素能受体参与对外源性NE的血管收缩反应，并且可能被内源性释放的NE激活。
