Borkowski K R, Quinn P
Br J Pharmacol. 1983 Nov;80(3):429-37. doi: 10.1111/j.1476-5381.1983.tb10712.x.
Bilateral adrenal demedullation of juvenile spontaneously hypertensive rats attenuated, but did not prevent, the development of hypertension. Neither did it affect the subsequent vascular reactivity to phenylephrine though it significantly reduced the vascular effects of sympathetic nerve stimulation. Demedullation of adult spontaneously hypertensive rats did not alter blood pressure, but did attenuate the pressor responses to both alpha-adrenoceptor agonists and sympathetic nerve stimulation. In acutely demedullated adult rats, vascular reactivity to sympathetic nerve stimulation, but not to exogenous amines, could be restored by slow i.v. infusion of adrenaline in a dose-dependent manner. The results support a possible facilitatory role for adrenaline in sympathetic neurotransmitter release, both during the development of genetic hypertension and in vascular responses to sympathetic nerve stimulation.
对幼年自发性高血压大鼠进行双侧肾上腺髓质剥除可减轻但不能阻止高血压的发展。它也不影响随后血管对去氧肾上腺素的反应性,尽管它显著降低了交感神经刺激的血管效应。对成年自发性高血压大鼠进行髓质剥除不会改变血压,但会减弱对α-肾上腺素能受体激动剂和交感神经刺激的升压反应。在急性髓质剥除的成年大鼠中,通过静脉缓慢输注肾上腺素,血管对交感神经刺激(而非对外源性胺类)的反应性可呈剂量依赖性恢复。这些结果支持了肾上腺素在遗传性高血压发展过程中以及在血管对交感神经刺激的反应中,可能在交感神经递质释放方面发挥促进作用。