Interaction of bradykinin and angiotensin in the regulation of blood pressure in conscious rats.

M van den Buuse, J Kerkhoff
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引用次数: 5

Abstract

1. The interaction between bradykinin (BK) and the renin-angiotensin system was studied in conscious, catheterized rats. 2. Intravenous injection of BK induced dose-dependent decreases in blood pressure in normotensive Wistar and Wistar-Kyoto rats and spontaneously hypertensive rats. Pretreatment with the angiotensin-converting enzyme (ACE) inhibitor captopril markedly enhanced the effect of BK, such that the dose-response curve shifted significantly to the left in all three strains. 3. In a second series of experiments, captopril did not change basal blood pressure, but blocked the pressor response to angiotensin I (AI), but not angiotensin II (AII). 4. The partial agonist Sar1-Ala8-angiotensin II (SAR) increased blood pressure and blocked the pressor response to subsequent AII treatment. 5. After pretreatment with BK (50 micrograms/kg), captopril evoked a decrease in blood pressure, while still blocking the effect of AI. 6. After pretreatment with BK, SAR decreased blood pressure, while still antagonizing the action of AII. 7. These results suggest that ACE plays a role in the inactivation of circulating BK in normotensive and hypertensive rats. Conversely, BK can influence the activity of the renin-angiotensin system, probably by interacting with ACE.

缓激素和血管紧张素在清醒大鼠血压调节中的相互作用。
1. 研究了缓激素(BK)与肾素-血管紧张素系统的相互作用。2. 静脉注射BK诱导正常Wistar、Wistar- kyoto大鼠和自发性高血压大鼠血压呈剂量依赖性下降。血管紧张素转换酶(ACE)抑制剂卡托普利(captopril)预处理显著增强了BK的作用,三种菌株的剂量-反应曲线均显著左移。3.在第二个系列实验中,卡托普利没有改变基础血压,但阻断了血管紧张素I (AI)的升压反应,而不是血管紧张素II (AII)。4. 部分激动剂sar1 - ala8 -血管紧张素II (SAR)升高血压,阻断对后续AII治疗的升压反应。5. 用BK(50微克/千克)预处理后,卡托普利引起血压下降,同时仍然阻断AI的作用。6. 经BK预处理后,SAR降低血压,同时仍能拮抗AII的作用。7. 这些结果表明,ACE在正常和高血压大鼠循环BK失活中起作用。相反,BK可能通过与ACE相互作用影响肾素-血管紧张素系统的活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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