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慢性钠耗竭会抑制最后区升压通路。

Chronic sodium depletion suppresses the area postrema pressor pathway.

作者信息

Szilagyi J E, Ferrario C M

出版信息

Life Sci. 1987 May 11;40(19):1915-20. doi: 10.1016/0024-3205(87)90051-8.

Abstract

Sodium depletion in dogs is known to affect both the renin-angiotensin as well as the sympathetic nervous system. The effect of this dietary regime upon the area postrema pressor pathway, as evaluated by the cardiovascular responses to centrally acting angiotensin II, has not been determined previously. With this in mind, male mongrel dogs were maintained on either a normal or a sodium restricted diet supplemented with furosemide and dose-response curves for intravertebral and intravenous angiotensin II (range: 1-20 ng/kg/min) were obtained. Sodium depletion results in not only a blunted intravenous pressor response to angiotensin II but also the abolition of the centrally mediated pressor responses mediated by the area postrema. Because accumulating evidence indicates that in sodium depleted dogs sympathetic nerve activity is reduced while central noradrenergic inhibitory activity is increased the reduced effects of angiotensin II upon the central sympathetically mediated pressor response may in part be related to decreases in sympathetic nerve activity.

摘要

已知犬体内的钠耗竭会影响肾素 - 血管紧张素以及交感神经系统。这种饮食方案对最后区升压途径的影响,此前尚未通过对中枢作用的血管紧张素II的心血管反应来评估。考虑到这一点,将雄性杂种犬维持在正常饮食或补充速尿的限钠饮食上,并获得了椎内和静脉注射血管紧张素II(范围:1 - 20 ng/kg/分钟)的剂量 - 反应曲线。钠耗竭不仅导致对血管紧张素II的静脉升压反应减弱,还消除了由最后区介导的中枢介导的升压反应。因为越来越多的证据表明,在钠耗竭的犬中,交感神经活动减少而中枢去甲肾上腺素能抑制活动增加,所以血管紧张素II对中枢交感神经介导的升压反应的作用减弱可能部分与交感神经活动的降低有关。

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