Chronic AT1 receptor blockade alters aortic nerve activity in hypertension.

Chronic AT1 receptor blockade alters aortic nerve activity in hypertension.
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慢性 AT1 受体阻断会改变高血压患者的主动脉神经活动。

DOI:
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发表时间:
1998
期刊:
影响因子:
8.3
通讯作者:
Brazil Correspondence
Brazil Correspondence
中科院分区:
医学1区
文献类型:
--
作者:
Cláudia M. dos Santos;E. Moreira;Eduardo M. Krieger;L. Michelini;Paulo;São Paulo;Brazil Correspondence

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在缩窄性高血压(CH)的慢性期,我们已经显示压力感受器敏感性降低(高血压。1992;19[suppl II]:II-198-II-201.)和心率的抑制压力感受器反射控制的正常化,即使在氯沙坦治疗的动物中高血压持续存在(Am J Physiol.1995;269:H812-H818)。在本研究中,我们分析了血管紧张素II阻滞对CH和假手术组的传入主动脉神经活动的影响,这些组长期接受溶媒或氯沙坦(每天10 mg/kg,p.o.)治疗。CH是通过动脉瓣下主动脉缩窄诱导的,并且处理持续8天(4个对照和4个实验天)。在实验期第四天记录主动脉压(清醒大鼠)和与压力同时的主动脉神经活动(麻醉大鼠)。氯沙坦治疗的大鼠显示尾压降低(104+/-3 mmHg vs溶媒组117+/-3 mmHg)。在两组中,与假手术缩窄动物相比,主动脉缩窄导致压力显著增加(分别为25%和28%)和主动脉神经活动/压力关系的抑制。在压力变化的生理范围内,氯沙坦治疗后抑郁明显较小(氯沙坦和溶媒治疗CH组分别为3.30+/-0.33 vs 2.18+/-0.37%/mmHg,假手术溶媒治疗组为5.05+/-0.33%/mmHg)。血管紧张素1型(AT 1)受体阻滞剂也伴随着传入放电的变异性降低。数据表明,除了其压力效应,血管紧张素II作用于AT 1受体,在生理(+/-10 mm Hg)压力升高和降低期间降低主动脉传入神经的敏感性。因此,血管紧张素II可能有助于减少慢性高血压的压力感受器增益。
In the chronic phase of coarctation hypertension (CH) we have shown both reduction in baroreceptor sensitivity (Hypertension. 1992;19[suppl II]:II-198-II-201.) and normalization of the depressed baroreceptor reflex control of heart rate, even with the persistence of hypertension in losartan-treated animals (Am J Physiol. 1995;269:H812-H818). In the present study we analyzed the effects of angiotensin II blockade on afferent aortic nerve activity of CH and sham-operated groups treated chronically with vehicle or losartan (10 mg/kg per day p.o.). CH was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 8 days (4 control and 4 experimental days). Aortic pressure (conscious rats) and aortic nerve activity simultaneous to pressure (anesthetized rats) were recorded on the fourth day of the experimental period. Losartan-treated rats showed reduced tail pressure (104+/-3 versus 117+/-3 mm Hg in the vehicle group). In both groups, aortic coarctation caused a significant increase in pressure (25% and 28%, respectively) and a depression of the aortic nerve activity/pressure relationship when compared with sham-operated coarcted animals. In the physiological range of pressure changes, the depression was significantly smaller after losartan treatment (3.30+/-0.33 versus 2.18+/-0.37%/mm Hg in the losartan- and vehicle-treated CH groups, respectively, versus 5.05+/-0.33%/mm Hg in the sham-operated vehicle-treated group). Angiotensin type 1 (AT1) receptor blockade was also accompanied by reduced variability of the afferent discharge. The data suggested that apart from its pressure effect, angiotensin II acts at AT1 receptors to decrease the sensitivity of aortic afferents during physiological (+/-10 mm Hg) increases and decreases in pressure. Thus, angiotensin II may contribute to reductions of baroreceptor gain in chronic hypertension.
AT1 受体在血管紧张素 II 重置兔心率压力反射控制中的作用。
DOI: 10.1172/jci116357
发表时间: 1993
期刊: The Journal of clinical investigation
影响因子: --
作者:
Wong,J;Chou,L;Reid,IA
通讯作者: Reid,IA
脑肾素-血管紧张素系统:定位和一般意义。
DOI: 10.1097/00005344-199219006-00010
发表时间: 1992
影响因子: 3
作者:
Bunnemann,B;Fuxe,K;Ganten,D
通讯作者: Ganten,D