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介导血管加压素心血管调节的中枢神经系统通路。

CNS pathways mediating cardiovascular regulation of vasopressin.

作者信息

Renaud L P

机构信息

Neurosciences, Loeb Research Institute, Ottawa Civic Hospital, Ontario, Canada.

出版信息

Clin Exp Pharmacol Physiol. 1996 Feb;23(2):157-60. doi: 10.1111/j.1440-1681.1996.tb02589.x.

Abstract
  1. The release of vasopressin from the neurohypophysial terminals of hypothalamic magnocellular neurosecretory neurons is subject to regulation by peripheral baroreceptors, cardiopulmonary volume receptors and circulating angiotensin II. Information from these sources is transmitted through different pathways to achieve different influences on the excitability of the vasopressin-secreting cells. 2. A brief increase in arterial pressure, sufficient to activate baroreceptors, is associated with a transient and selective GABAergic inhibition of these neurosecretory neurons, achieved through a multisynaptic pathway that involves ascending catecholaminergic fibres and neurons in the diagonal band of Broca. A decrease in arterial pressure activates peripheral low volume receptors and initiating neural inputs that result in an increase in the excitability of vasopressin-secreting neurons, achieved via pathways that include direct projections from caudal ventrolateral medulla A1 neurons. 3. Hypotension also releases renal renin and leads to the formation of angiotensin II; binding of this hormone to AT1 receptors on subfornical organ neurons promotes activation of a central angiotensinergic input that evokes a predominantly excitatory effect on vasopressin neurons.
摘要
  1. 下丘脑大细胞神经分泌神经元神经垂体终末释放血管加压素受外周压力感受器、心肺容量感受器和循环中的血管紧张素II调节。来自这些来源的信息通过不同途径传递,对血管加压素分泌细胞的兴奋性产生不同影响。2. 足以激活压力感受器的动脉压短暂升高,与这些神经分泌神经元的短暂性、选择性GABA能抑制相关,这是通过一条多突触途径实现的,该途径涉及上升的儿茶酚胺能纤维和布罗卡斜带中的神经元。动脉压降低会激活外周低容量感受器并启动神经输入,导致血管加压素分泌神经元兴奋性增加,并通过包括尾侧腹外侧延髓A1神经元的直接投射在内的途径实现。3. 低血压还会释放肾素并导致血管紧张素II形成;该激素与穹窿下器官神经元上的AT1受体结合,促进中枢血管紧张素能输入的激活,对血管加压素神经元产生主要为兴奋性的作用。

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