Aubert J F, Waeber B, Nussberger J, Vavrek R, Stewart J M, Brunner H R
Division of Hypertension, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
J Cardiovasc Pharmacol. 1988 Jan;11(1):51-5. doi: 10.1097/00005344-198801000-00008.
The present study was designed to assess in conscious normotensive rats the influence of various pressor agents on the acute blood pressure response to a bradykinin antagonist (B4162). This antagonist was used at a dose (400 micrograms i.v.) which had been previously shown to block the blood pressure lowering effect of exogenous bradykinin for several minutes. In control rats, the bradykinin antagonist had no effect on blood pressure. However, in rats pretreated with nonpressor doses of angiotensin II or methoxamine or with pressor doses of vasopressin or methoxamine, the same antagonist significantly increased blood pressure by 10 +/- 2.2, 12 +/- 2.7, 9 +/- 1.7, and 16 +/- 3.4 mm Hg, respectively. It therefore appears that circulating bradykinin is not directly involved in blood pressure regulation of conscious normotensive rats. Endogenous bradykinin may however play an important role in blood pressure control by attenuating the pressor effect of angiotensin II, vasopressin, and alpha-adrenoceptor stimulation.
本研究旨在评估在清醒的正常血压大鼠中,各种升压剂对缓激肽拮抗剂(B4162)急性血压反应的影响。该拮抗剂静脉注射剂量为400微克,此前已证明该剂量能在几分钟内阻断外源性缓激肽的降压作用。在对照大鼠中,缓激肽拮抗剂对血压无影响。然而,在用非升压剂量的血管紧张素II或甲氧明预处理的大鼠中,或在用升压剂量的血管加压素或甲氧明预处理的大鼠中,相同的拮抗剂分别使血压显著升高10±2.2、12±2.7、9±1.7和16±3.4毫米汞柱。因此,似乎循环中的缓激肽并不直接参与清醒正常血压大鼠的血压调节。然而,内源性缓激肽可能通过减弱血管紧张素II、血管加压素和α-肾上腺素能受体刺激的升压作用,在血压控制中发挥重要作用。