Effects of Angiotensin Infusion on Catecholamine Uptake and Reactivity in Blood Vessels
Effects of Angiotensin Infusion on Catecholamine Uptake and Reactivity in Blood Vessels
复制标题
血管紧张素输注对儿茶酚胺摄取和血管反应性的影响
作者：
P. Khairallah;D. Davila;N. Papanicolaou;N. Glende;P. Meyer
本文研究了大鼠血管紧张素与儿茶酚胺摄取的相互关系。血管紧张素以3种剂量水平输注5、30或120分钟：1、12和45 ng/kg/min。短期暴露于血管紧张素，在肾脏、子宫和肾上腺中观察到影响。这些器官先前已显示出结合静脉内施用的最大量的氚化肽。在5分钟和30分钟实验中，血管紧张素抑制了大部分组织中间羟胺或去甲肾上腺素的摄取，尤其是在较高剂量水平下，肾上腺除外，肾上腺的摄取增加。输注2小时后，在大多数器官中观察到摄取抑制。当静脉注射高滴度血管紧张素II抗体时，对静脉注射血管紧张素的反应被取消。在这个阶段，肾脏、心脏、脾脏和输精管对氚化去甲肾上腺素的摄取增加，而肾上腺的摄取减少。为了了解这些生化发现是否与生理作用有关，研究了兔离体灌注动脉的收缩反应。血管紧张素增强灌注压的增加后，输注去甲肾上腺素，而血管紧张素II抗体降低这种反应。因此，可以得出结论，血管紧张素可以修改的摄取，因此，失活的交感神经递质，并可能通过这种机制改变去甲肾上腺素和交感神经刺激的生理反应。
The interrelations between angiotensin and catecholamine uptake have been studied in rats. Angiotensin was infused for either 5, 30, or 120 minutes at three dose levels: 1, 12, and 45 ng/kg/min. With short exposures to angiotensin, effects were seen in kidney, uterus, and adrenal gland. These organs had been previously shown to bind the greatest amount of tritiated peptide administered intravenously. In the 5- and 30-minute experiments angiotensin inhibited uptake of either metaraminol or norepinephrine in most tissues, especially at the higher dose levels, with the exception of the adrenal gland where uptake was increased. After the two-hour infusion inhibition of uptake was seen in most organs. When high titer angiotensin II antibodies were administered intravenously, responses to iv angiotensin were abolished. At this stage the uptake of tritiated norepinephrine was increased in kidney, heart, spleen, and vas deferens, while it was decreased in the adrenal gland. To see whether these biochemical findings are related to a physiological role, contractile responses of isolated perfused arteries of rabbits were studied. Angiotensin potentiated the increase in perfusion pressure after the infusion of norepinephrine, while angiotensin II antibodies decreased this response. Thus, it is concluded that angiotensin can modify the uptake and, hence, the inactivation of the sympathetic neurotransmitter and possibly by this mechanism alter the physiological response to norepinephrine and sympathetic stimulation.