Haberl R L, Decker-Hermann P J, Hermann K
Department of Neurology, University of Munich, Germany.
J Cereb Blood Flow Metab. 1996 Jul;16(4):714-9. doi: 10.1097/00004647-199607000-00023.
There is evidence of an intrinsic renin-angiotensin system in the brain. The goal of the study was to determine whether stimulation of endogenous angiotensin production by applying renin to the brain surface has an effect on pial arteriolar caliber and CBF. Pial vessel diameters were measured through a closed cranial window in anesthetized rabbits. Percent changes of blood flow in the cortical area under the cranial window were simultaneously measured by laser-Doppler flowmetry. Topical application of 0.01-0.1 U/ml renin induced maximum dilation of 18.9 +/- 4% (mean +/- SD) of pial arterioles within 2 min. Arteriolar calibers thereafter decreased slowly. Flow gradually increased to peak at 38 +/- 15% 50 min after renin application. Angiotensin I levels in jugular blood, as measured by radioimmunoassay, increased to a peak 40 min after topical renin application. Angiotensin II levels in jugular blood and both angiotensin I and II levels in blood samples from the femoral artery did not change. Diameter and flow changes were inhibited by intravenous pretreatment with the converting enzyme blocker captopril (10 mg/kg body wt i.v.). Captopril did not affect the vasodilation and flow increase in response to hypercapnia. Topically applied captopril (10(-5) M) blocked renin-induced arteriolar dilation. We conclude that renin increases pial arteriolar diameters and cortical blood flow in the rabbit brain. Stimulation of angiotensin production is likely to be a mediator of this response.
有证据表明大脑中存在内源性肾素-血管紧张素系统。本研究的目的是确定通过将肾素应用于脑表面来刺激内源性血管紧张素生成是否会对软脑膜小动脉管径和脑血流量产生影响。在麻醉的兔子中通过闭合的颅骨视窗测量软脑膜血管直径。同时用激光多普勒血流仪测量颅骨视窗下皮质区域的血流百分比变化。局部应用0.01 - 0.1 U/ml肾素在2分钟内可使软脑膜小动脉最大扩张18.9±4%（平均值±标准差）。此后小动脉管径缓慢减小。血流在应用肾素后50分钟逐渐增加至峰值，增幅为38±15%。通过放射免疫测定法测得的颈静脉血中血管紧张素I水平在局部应用肾素后40分钟升至峰值。颈静脉血中血管紧张素II水平以及股动脉血样中血管紧张素I和II水平均未改变。静脉内预先给予转化酶阻滞剂卡托普利（10 mg/kg体重静脉注射）可抑制管径和血流变化。卡托普利不影响对高碳酸血症的血管舒张和血流增加反应。局部应用卡托普利（10⁻⁵ M）可阻断肾素诱导的小动脉扩张。我们得出结论，肾素可增加兔脑软脑膜小动脉管径和皮质血流量。血管紧张素生成的刺激可能是这种反应的介导因素。
