Woo N D, Mukherjee K, Ganguly P K
Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
Am J Physiol. 1993 Sep;265(3 Pt 2):H893-8. doi: 10.1152/ajpheart.1993.265.3.H893.
Recent evidence supports the view that the sympathetic system actively participates in the development of hypertension. Because norepinephrine, contained within central neurons involved in cardiovascular sympathetic regulation, is known to coexist with neuropeptide Y, it is possible that a functional interaction between neuropeptide Y and norepinephrine exists within the brain. In an effort to clarify whether or not central catecholamine systems are modulated by neuropeptide Y in hypertensive situations, the paraventricular nucleus of spontaneously hypertensive rats was exposed to neuropeptide Y (10(-9) M), and levels of norepinephrine were sampled by microdialysis. Norepinephrine levels in spontaneously hypertensive rats were significantly increased and did not change after exposure to neuropeptide Y, in sharp contrast to the decreases seen in Wistar-Kyoto controls. To ascertain whether these alterations in norepinephrine control were specific to the model used, a similar series of experiments was carried out in the paraventricular nucleus of aortic-banded rats. These studies supported the previous findings. Norepinephrine levels in aortic-banded rats were markedly elevated when compared with sham-operated controls and demonstrated no change after exposure to neuropeptide Y, whereas decreases of > 50% were seen in sham-operated controls. These results support the view that mechanisms normally involving neuropeptide Y as a neuromodulator in the paraventricular nucleus are altered in hypertensive situations. It is suggested that hypertension may precipitate changes in mechanisms involving brain neuropeptide Y and increased sympathetic activity.
最近的证据支持这样一种观点,即交感神经系统积极参与高血压的发展。因为已知参与心血管交感神经调节的中枢神经元中所含的去甲肾上腺素与神经肽Y共存,所以大脑中神经肽Y和去甲肾上腺素之间可能存在功能相互作用。为了阐明在高血压情况下中枢儿茶酚胺系统是否受神经肽Y调节,将自发性高血压大鼠的室旁核暴露于神经肽Y(10⁻⁹ M),并通过微透析对去甲肾上腺素水平进行采样。自发性高血压大鼠的去甲肾上腺素水平显著升高,暴露于神经肽Y后没有变化,这与Wistar-Kyoto对照大鼠中观察到的下降形成鲜明对比。为了确定去甲肾上腺素控制的这些改变是否特定于所使用的模型,在主动脉缩窄大鼠的室旁核中进行了一系列类似的实验。这些研究支持了先前的发现。与假手术对照相比,主动脉缩窄大鼠的去甲肾上腺素水平显著升高,暴露于神经肽Y后没有变化,而假手术对照大鼠的去甲肾上腺素水平下降超过50%。这些结果支持这样一种观点,即在高血压情况下,通常涉及神经肽Y作为室旁核神经调节剂的机制发生了改变。有人提出,高血压可能促使涉及脑内神经肽Y的机制发生变化,并增加交感神经活动。