Borkowski K R, Porter M
J Auton Pharmacol. 1983 Dec;3(4):275-9. doi: 10.1111/j.1474-8673.1983.tb00545.x.
Pressor responses to bolus injections of noradrenaline (NA) were studied, in the isolated perfused rat mesenteric arterial bed, in the presence of beta-adrenoreceptor agonists and antagonists, in an attempt to identify a possible beta-adrenoreceptor mediated modulation of catecholamine-induced vasoconstrictor effects. NA-induced responses were potentiated in the presence of timolol and (-)propranolol and suppressed in the presence of (-)isoprenaline; (+)isoprenaline was less effective against the NA-induced responses. Timolol attenuated the effects of (-)isoprenaline on NA-induced responses but not those of the stereoisomer (+)isoprenaline. It is concluded that the NA-induced pressor effect in the rat mesenteric vasculature is the net result of vasoconstrictor alpha- and vasodilator beta-adrenoreceptor activation and that the interaction of the two opposing adrenoreceptor-mediated effects represents a 'physiological antagonism'.
在离体灌注的大鼠肠系膜动脉床中，研究了在存在β-肾上腺素能受体激动剂和拮抗剂的情况下，对去甲肾上腺素（NA）推注的升压反应，以试图确定一种可能的β-肾上腺素能受体介导的儿茶酚胺诱导的血管收缩作用的调节。在噻吗洛尔和（-）普萘洛尔存在下，NA诱导的反应增强，而在（-）异丙肾上腺素存在下则受到抑制；（+）异丙肾上腺素对NA诱导的反应效果较差。噻吗洛尔减弱了（-）异丙肾上腺素对NA诱导反应的作用，但对立体异构体（+）异丙肾上腺素的作用没有影响。得出的结论是，大鼠肠系膜血管系统中NA诱导的升压作用是血管收缩性α-和血管舒张性β-肾上腺素能受体激活的净结果，并且这两种相反的肾上腺素能受体介导的作用之间的相互作用代表了一种“生理性拮抗”。
