Buñag R D, Eriksson L, Tanabe S
Department of Pharmacology, College of Health Sciences and Hospital, University of Kansas Medical Center, Kansas City 66103.
Hypertension. 1990 Mar;15(3):284-90. doi: 10.1161/01.hyp.15.3.284.
Involvement of the brain renin-angiotensin system in baroreceptor reflex regulation was assessed by recording reflex heart rate and sympathetic nerve responses in normotensive rats that had been infused intracerebroventricularly with the converting enzyme inhibitor enalapril for 15 days. Reflex bradycardia and sympathetic nerve inhibition during pressor responses to phenylephrine were larger in rats with intracerebroventricularly infused enalapril than in control rats similarly infused either intracerebroventricularly with saline or intravenously with enalapril. In contrast, opposite reflex responses to sodium nitroprusside-induced hypotension were mostly unaffected. Because depressor, bradycardic, and sympathoinhibitory responses to electrical stimulation of the central cut end of the left aortic depressor nerve were also enhanced, intracerebroventricularly infused enalapril must be affecting the baroreceptor reflex arc centrally. These results are compatible with the interpretation that intracerebroventricularly infused enalapril enhanced baroreceptor reflex sensitivity by reducing endogenous angiotensin II levels in the brain through converting enzyme inhibition.
通过记录正常血压大鼠的反射性心率和交感神经反应，评估脑肾素-血管紧张素系统在压力感受器反射调节中的作用。这些大鼠脑室内注入转化酶抑制剂依那普利15天。与脑室内注入生理盐水或静脉内注入依那普利的对照大鼠相比，脑室内注入依那普利的大鼠对去氧肾上腺素升压反应时的反射性心动过缓和交感神经抑制作用更大。相反，对硝普钠诱导的低血压的相反反射反应大多未受影响。由于对左主动脉减压神经中枢切断端电刺激的降压、心动过缓和交感神经抑制反应也增强，脑室内注入依那普利必定在中枢影响压力感受器反射弧。这些结果符合以下解释：脑室内注入依那普利通过转化酶抑制降低脑内内源性血管紧张素II水平，从而增强压力感受器反射敏感性。
