Saavedra J M, Grobecker H, Axelrod J
Circ Res. 1978 Apr;42(4):529-34. doi: 10.1161/01.res.42.4.529.
Catecholamines and catecholamine-synthesizing enzymes have been examined in specific brain areas during the development of spontaneously (genetic) hypertensive (SH) rats. Changes in catecholamine metabolism were localized to regions of the brain implicated in the regulation of blood pressure. Norepinephrine levels and dopamine-beta-hydroxylase (DBH) activities were decreased in specific nuclei of the hypothalamus and in the nucleus interstitialis striae terminalis ventralis, in both young and adult rats. The decrease in the formation of norepinephrine can result in a reduced activation of central alpha-adrenergic receptors which may be related causally to the onset of hypertension. The activity of the epinephrine-forming enzyme, phenylethanolamine-N-methyltransferase (PNMT), was increased in the A1 and A2 areas of the brainstem in young SH rats, but it was normal in adult hypertensive animals. These results implicate adrenergic neurons in the brainstem and noradrenergic neurons in the hypothalamus in the development of spontaneous (genetic) hypertension in rats.
在自发性（遗传性）高血压（SH）大鼠的发育过程中，已对特定脑区中的儿茶酚胺和儿茶酚胺合成酶进行了检测。儿茶酚胺代谢的变化定位于与血压调节有关的脑区。在幼年和成年大鼠的下丘脑特定核团以及终纹床核腹侧间质核中，去甲肾上腺素水平和多巴胺-β-羟化酶（DBH）活性均降低。去甲肾上腺素生成减少会导致中枢α-肾上腺素能受体的激活减少，这可能与高血压的发病存在因果关系。在幼年SH大鼠的脑干A1和A2区域，肾上腺素形成酶苯乙醇胺-N-甲基转移酶（PNMT）的活性增加，但在成年高血压动物中该活性正常。这些结果表明，大鼠自发性（遗传性）高血压的发生与脑干中的肾上腺素能神经元以及下丘脑中的去甲肾上腺素能神经元有关。
