Kuchel O, Racz K, Debinski W, Gutkowska J, Buu N T, Cantin M, Genest J
Laboratory of the Autonomic Nervous System, Hôtel-Dieu Hôpital, Montréal, Que., Canada.
Can J Physiol Pharmacol. 1987 Aug;65(8):1690-6. doi: 10.1139/y87-265.
We have previously demonstrated two different catecholaminergic patterns in genetic and experimental hypertension: a hyperdopaminergic state in spontaneously hypertensive (Okamoto) rats (SHR) and a hypernoradrenergic state in salt-sensitive Dahl rats. Plasma immunoreactive atrial natriuretic factor (IR ANF) concentrations increase in both models as a response to hypertension. To distinguish between the genetic and acquired components of these abnormalities, we measured adrenal dopamine-beta-hydroxylase (D beta H) activity and coeliac ganglionic atrial natriuretic factor (ANF) like immunoreactivity in the two animal strains. While adrenal D beta H activity was increased in Dahl S rats, it was diminished in SHR in the prehypertensive as well as in the hypertensive stages. In the hypertensive stage, the ANF-like immunoreactivity in the coeliac ganglia was lower in the Dahl S group but higher in SHR than in their respective normotensive controls; there were no changes in these animals when they were prehypertensive. Differences in D beta H activity, which determines the fine tuning of sympathoadrenomedullary catecholamine synthesis may account for the inheritance of mechanisms resulting in salt-sensitive hypertension (as in SHR) or salt-dependent hypertension (as in Dahl salt-sensitive rats). In contrast, plasma IR ANF concentrations may reflect a defense mechanism against hypertension. However ANF-like immunoreactivity in coeliac ganglia does not follow its plasma concentrations and changes in different directions in the two hypertensive strains; it may reflect a neuromodulatory function of ANF in the ganglionic neurotransmission and different implications of this role of ANF in the two hypertensive models.
自发性高血压（冈本）大鼠（SHR）呈现高多巴胺能状态，而盐敏感型 Dahl 大鼠呈现高去甲肾上腺素能状态。在这两种模型中，作为对高血压的反应，血浆免疫反应性心房利钠因子（IR ANF）浓度均升高。为了区分这些异常的遗传和后天成分，我们测量了两种动物品系的肾上腺多巴胺-β-羟化酶（DβH）活性以及腹腔神经节中类似心房利钠因子（ANF）的免疫反应性。虽然 Dahl S 大鼠的肾上腺 DβH 活性增加，但在高血压前期和高血压阶段，SHR 的该活性均降低。在高血压阶段，Dahl S 组腹腔神经节中类似 ANF 的免疫反应性低于 SHR，但高于各自的正常血压对照；在高血压前期，这些动物没有变化。DβH 活性的差异决定了交感肾上腺髓质儿茶酚胺合成的精细调节，这可能解释了导致盐敏感性高血压（如 SHR）或盐依赖性高血压（如 Dahl 盐敏感大鼠）的机制的遗传性。相比之下，血浆 IR ANF 浓度可能反映了一种对抗高血压的防御机制。然而，腹腔神经节中类似 ANF 的免疫反应性并不随其血浆浓度变化，且在两种高血压品系中变化方向不同；它可能反映了 ANF 在神经节神经传递中的神经调节功能以及 ANF 在两种高血压模型中该作用的不同影响。
