ROLE OF BRADYKININ IN THE REGULATION OF BLOOD PRESSURE AND RENAL HEMODYNAMICS.

为了探讨内源性缓激肽在调节血压（BP）和肾血流（RBF）中的可能作用，我们在麻醉的SD大鼠、自发性高血压大鼠（SHR）、DOCA盐性高血压大鼠和日本白化兔中研究了缓激肽的竞争拮抗剂（B4147）。在SD大鼠中，静脉输注B4147可抑制外源性缓激肽69%的抑制作用。SD大鼠注射25 ~ 100马克B4147后，血压升高，RBF降低，呈剂量依赖性。血管紧张素11拮抗剂或α _1受体阻滞剂不能阻断血压升高。卡托普利可显著降低血压。然而，在卡托普利给药后注射B4147引起的血压升高是卡托普利最初引起的血压下降的43%。这些结果表明，B4147对血压和RBF的影响不是通过血管紧张素11或交感alpha_1刺激介导的。外源性缓激肽可能有助于SD大鼠血压和RBF的维持。此外，缓激肽可能部分参与转化酶抑制剂卡托普利诱导的急性降压作用。SHR组血压变化幅度明显低于对照组（WKY）。WKY组RBF的减少幅度大于SHR组。缓激素有助于维持两种菌株的BP和RBF。然而，SHR中缓激肽系统的缺乏可能在一定程度上促进了高血压的发展或维持。在DOCA高血压大鼠中，血压升高幅度明显低于DOCA高血压大鼠。与对照组相比，DOCA高血压大鼠RBF下降幅度减小。这些结果表明，内源性缓激肽在doca高血压大鼠的高血压建立期被抑制。在麻醉家兔肾动脉内给予缓激肽拮抗剂后，RBF和GFR均显著降低。这些结果提示内源性激肽可能参与RBF和GFR的调控。少

To examine a possible role of endogenous bradykinin in the regulation of blood pressure(BP) and renal blood flow(RBF), a competitive antagonist of bradykinin(B4147) was studied in anesthetized Sprague Dawley(SD) rats, spontaneously hypertensive rats(SHR), DOCA salt hypertensive rats and Japanese albino rabbits. In SD rats, the intravenous infusion of B4147 inhibited the depressor effect of exogenous bradykinin by 69%. After an injection of B4147 at a dose of 25-100 mug in SD rats, BP increased and RBF decreased in a dose dependent fashion. The increase in BP was not blocked by treatment with angiotensin 11 antagonist or alpha_1-blocker. The administration of captopril decreased BP significantly. However, the injection of B4147 after the administration of captopril elicited an increase in BP of 43% of the initial decrease induced by captopril. These results suggest that the effects of B4147 on BP and RBF are not mediated through angiotensin 11 or sympathetic alpha_1-stimulation. Exogeno … More us bradykinin could contribute to the maintenance of BP and RBF in SD rats. Furthermore, bradykinin may partly participate in the acute hypotensive effect induced by the converting enzyme inhibitor captopril. In SHR, the magnitude in the change in BP was significantly lower in SHR than in control(WKY). The reduction of RBF was greater in WKY than in SHR. Bradykinin contributes to the maintenance of BP and RBF in both strains. However, deficiency in the bradykinin system in SHR may contributes partly to the development or the maintenance of hypertension. In DOCA-hypertensive rats, the magnitude of the increase in BP was significantly lower in DOCA hypertensive rats. The extent of the fall in RBF was reduced in DOCA hypertensive rats compared with control. These results suggest that endogenous bradykinin is depressed in the established phase of hypertension in DOCA-hypertensive rats. After the administration of bradykinin antagonist into the renal artery in anesthetized rabbits, both RBF and GFR were decreased significantly. These results indicate that endogenous kinins may participate in the regulation of RBF and GFR. Less