Rowe B P
Clin Exp Hypertens A. 1984;6(7):1281-95. doi: 10.3109/10641968409039597.
The contribution of vasodilator prostaglandins and kinins to blood pressure regulation was studied during the infusion of different doses of angiotensin II in conscious rabbits. Angiotensin II was infused for 60 min. in each experiment. Indomethacin, a prostaglandin synthesis inhibitor, or Trasylol, a kallikrein inhibitor, was given at the 30 min. interval. Indomethacin caused a sustained increase in blood pressure during the infusion of pressor doses of angiotensin II. The range of the mean increase after prostaglandin synthesis inhibition was 3.4 to 6.0 and 3.0 to 9.4 mm Hg at angiotensin II infusion rates of 10 and 50 ng/kg/min respectively. In contrast, indomethacin did not alter blood pressure when the peptide was administered at subpressor levels. Trasylol did not alter blood pressure during infusion of angiotensin II. These results suggest that when blood pressure is maintained at supranormal levels by angiotensin II, the pressor action is attenuated by one or more prostaglandins; an event which is not mediated or assisted by changes in kinin metabolism.
在清醒家兔输注不同剂量血管紧张素II的过程中,研究了血管舒张性前列腺素和激肽对血压调节的作用。每次实验中血管紧张素II输注60分钟。在30分钟时给予前列腺素合成抑制剂吲哚美辛或激肽释放酶抑制剂抑肽酶。在输注升压剂量的血管紧张素II期间,吲哚美辛使血压持续升高。在血管紧张素II输注速率分别为10和50 ng/kg/min时,前列腺素合成抑制后平均血压升高范围分别为3.4至6.0 mmHg和3.0至9.4 mmHg。相比之下,当以低于升压水平给予该肽时,吲哚美辛不会改变血压。在输注血管紧张素II期间,抑肽酶不会改变血压。这些结果表明,当血管紧张素II将血压维持在超常水平时,一种或多种前列腺素会减弱升压作用;这一事件并非由激肽代谢变化介导或辅助。