Bomtempo C A, Santos G F, Santos R A, Campagnole-Santos M J
Departamento de Fisiologia e Biofisica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Brazil.
J Hypertens. 1998 Dec;16(12 Pt 1):1797-804. doi: 10.1097/00004872-199816120-00013.
Previous studies have shown that angiotensin-(1-7) potentiates the vascular actions of bradykinin. In the present study, we evaluated the interaction of bradykinin and angiotensin-(1-7) in the central modulation of baroreflex control of the heart rate.
Blood pressure and reflex bradycardia, elicited by intravenous injection of phenylephrine, were evaluated in conscious male Wistar rats before and at the end of 1 h of an intracerebroventricular infusion of angiotensin-(1-7) at 0.5 or 1.0 microg/h combined with bradykinin at 2.5 microg/h; or angiotensin-(1-7) at 2.0 microg/h combined with bradykinin at 4.0 microg/h; or angiotensin-(1-7) alone at 2.0 or 4.0 microg/h; or bradykinin alone at 4.0 or 8.0 microg/h; or saline at 8 microl/h. In addition, baroreflex bradycardia was evaluated before and at the end of 1 and 2 h of intracerebroventricular infusion of angiotensin-(1-7) at 4 microg/h for 2 h; or saline at 8 microl/h in the first hour followed by HOE 140 at 90 ng/h in the second hour; or angiotensin-(1-7) at 4 microg/h in the first hour followed by angiotensin-(1-7) at 4 microg combined with HOE 140 at 90 ng/h in the second hour; or HOE 140 at 90 ng/h in the first hour followed by HOE 140 at 90th ng/h combined with angiotensin-(1-7) at 4 microg/h in the second hour; or saline at 8 microl/h for 2 h.
The intracerebroventricular infusion of angiotensin-(1-7) or bradykinin alone required a dose of 4.0 and 8.0 microg/h, respectively, to facilitate baroreflex control of the heart. However, a simultaneous infusion of these peptides at subeffective rates was able to produce a significant increase in baroreflex sensitivity. In addition, the facilitation of the baroreflex control of the heart rate induced by angiotensin-(1-7) at 4.0 microg/h was inhibited by HOE 140.
These results suggest that centrally, bradykinin and angiotensin-(1-7) can interact in order to modulate baroreflex control of the heart rate. In addition, our data indicate that the central modulatory effect of angiotensin-(1-7) on the baroreflex is mediated, at least in part, by the release of kinins.
先前的研究表明，血管紧张素 -（1 - 7）可增强缓激肽的血管作用。在本研究中，我们评估了缓激肽与血管紧张素 -（1 - 7）在心率压力反射控制的中枢调节中的相互作用。
在清醒雄性Wistar大鼠中，静脉注射去氧肾上腺素诱发血压和反射性心动过缓，在脑室内以0.5或1.0微克/小时的速率输注血管紧张素 -（1 - 7）并联合2.5微克/小时的缓激肽；或以2.0微克/小时的血管紧张素 -（1 - 7）联合4.0微克/小时的缓激肽；或以2.0或4.0微克/小时单独输注血管紧张素 -（1 - 7）；或以4.0或8.0微克/小时单独输注缓激肽；或以8微升/小时输注生理盐水1小时之前和结束时进行评估。此外，在脑室内以4微克/小时的速率输注血管紧张素 -（1 - 7）2小时的1小时和2小时之前及结束时评估压力反射性心动过缓；或以8微升/小时输注生理盐水1小时，随后在第2小时以90纳克/小时输注HOE 140；或以4微克/小时的血管紧张素 -（1 - 7）在第1小时，随后在第2小时以4微克的血管紧张素 -（1 - 7）联合90纳克/小时的HOE 140；或以90纳克/小时的HOE 140在第1小时，随后在第2小时以90纳克/小时的HOE 140联合4微克/小时的血管紧张素 -（1 - 7）；或以8微升/小时输注生理盐水2小时进行评估。
单独脑室内输注血管紧张素 -（1 - 7）或缓激肽分别需要4.0和8.0微克/小时的剂量才能促进对心脏的压力反射控制。然而，以亚有效速率同时输注这些肽能够使压力反射敏感性显著增加。此外，HOE 140可抑制4.0微克/小时的血管紧张素 -（1 - 7）诱导的心率压力反射控制的促进作用。
这些结果表明，在中枢，缓激肽和血管紧张素 -（1 - 7）可以相互作用以调节心率的压力反射控制。此外，我们的数据表明，血管紧张素 -（1 - 7）对压力反射的中枢调节作用至少部分是由激肽的释放介导的。
