Weissinger J, Bloor C
Artery. 1980;7(2):123-38.
Concentration-contractile response curves for the thoracic (TA) and abdominal (AbA) aortae from spontaneously hypertensive (SHR) and normotensive control (WKY) rats were determined using adrenergic agonists. The concentrations of epinephrine (E) and norepinephrine (NE) necessary to produce a maximum response in the WKY TA were 7.07 x 10(-7) M and 1.68 x 10(-6) M, respectively. At greater concentrations TA responded with progressive relaxation. When similarly tested, SHR TA responded with significantly less relaxation. The concentrations of E and NE necessary to produce a maximum response in the WKY AbA were greater than 1.0 x 10(-5) M. No significant relaxation occurred at greater concentrations. The relaxation responses of the SHR AbA were no different than their normotensive controls. When propranolol was used the results suggested that relaxation is mediated by the beta-adrenoreceptor. The use of the beta 2-agonist, salbutamol, confirms the hypothesis that relaxation occurring in response to high concentrations of NE and E is partly a beta 2-adrenoeceptor phenomenon, and that this beta 2-adrenergic response decreases with early hypertension in TA. The different response patterns produced may partially account for the diversity of results regarding vascular sensitivity to vasoactive agents in the literature.
使用肾上腺素能激动剂测定了自发性高血压大鼠（SHR）和正常血压对照大鼠（WKY）胸主动脉（TA）和腹主动脉（AbA）的浓度-收缩反应曲线。在WKY TA中产生最大反应所需的肾上腺素（E）和去甲肾上腺素（NE）浓度分别为7.07×10⁻⁷ M和1.68×10⁻⁶ M。在更高浓度下，TA出现渐进性舒张反应。当进行类似测试时，SHR TA的舒张反应明显较弱。在WKY AbA中产生最大反应所需的E和NE浓度大于1.0×10⁻⁵ M。在更高浓度下未出现明显舒张。SHR AbA的舒张反应与其正常血压对照无差异。使用普萘洛尔时，结果表明舒张是由β-肾上腺素能受体介导的。使用β₂激动剂沙丁胺醇证实了以下假设：对高浓度NE和E产生的舒张部分是β₂-肾上腺素能受体现象，并且这种β₂-肾上腺素能反应在TA早期高血压时会降低。所产生的不同反应模式可能部分解释了文献中关于血管对血管活性药物敏感性的结果多样性。
