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B and C types natriuretic peptides modulate norepinephrine uptake and release in the rat hypothalamus.

机译:B型和C型利钠肽调节大鼠下丘脑中去甲肾上腺素的摄取和释放。

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We previously reported that atrial natriuretic factor (ANF) regulates catecholamine metabolism in the central nervous system. ANF, B and C types natriuretic peptides (BNP and CNP) also play a regulatory role in body fluid homeostasis, cardiovascular activity and hormonal and neuro-hormonal secretions. The aim of the present work was to investigate BNP and CNP effects on the uptake and release of norepinephrine (NE) in rat hypothalamic slices incubated in vitro. Results showed that BNP (100 nM) and CNP (1, 10 and 100 nM) enhanced total and neuronal [3H]NE uptake but did not modify non-neuronal uptake. BNP (100 nM) and CNP (1 nM) caused a rapid increase in NE uptake (1 min), which was sustained for 60 min. BNP (100 nM) did not modify the intracellular distribution of NE; however, 1 nM CNP increased the granular store and decreased the cytosolic pool of NE. BNP (100 nM) and CNP (1, 10 and 100 nM), diminished spontaneous NE release. In addition, BNP (1, 10, 100 nM) and CNP (1, 10 and 100 pM, as well as 1, 10 and 100 nM) reduced NE output induced by 25 mM KCl. These results suggest that BNP and CNP may be involved in the regulation of several central as well as peripheral physiological functions through the modulation of noradrenergic neurotransmission at the presynaptic neuronal level. Present results provide evidence to consider CNP as the brain natriuretic peptide since physiological concentrations of this peptide (pM) diminished NE evoked release.
机译:我们先前曾报道心房利钠因子(ANF)调节中枢神经系统中的儿茶酚胺代谢。 ANF,B和C型利尿钠肽(BNP和CNP)在体液稳态,心血管活动以及激素和神经激素分泌中也起调节作用。本工作的目的是研究BNP和CNP对在体外培养的大鼠下丘脑片中去甲肾上腺素(NE)摄取和释放的影响。结果显示,BNP(100 nM)和CNP(1、10和100 nM)增强了总和神经元[3H] NE的摄取,但未改变非神经元的摄取。 BNP(100 nM)和CNP(1 nM)导致NE摄取迅速增加(1分钟),持续60分钟。 BNP(100 nM)不会改变NE的胞内分布;然而,1 nM CNP增加了颗粒状储存并减少了NE的胞质池。 BNP(100 nM)和CNP(1、10和100 nM)减少了自发性NE释放。此外,BNP(1、10、100 nM)和CNP(1、10和100 pM,以及1、10和100 nM)降低了25 mM KCl诱导的NE输出。这些结果表明,BNP和CNP可能在突触前神经元水平上通过调节去甲肾上腺素能神经传递来参与几种中枢和外周生理功能的调节。目前的结果提供了将CNP视为脑利钠肽的证据,因为该肽(pM)的生理浓度降低了NE诱发的释放。

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