High salt intake is able to evoke neuroendocrine and autonomic responses that include vasopressin release and sympathoexcitation resulting in increasing in the arterial blood pressure (BP). The C1 neurons are a specific population of catecholaminergic neurons located in the RVLM region and they control BP under homeostatic imbalance. Thus, here we hypothesized that the ablation of C1 neurons mitigate the high blood pressure induced by high-salt intake. To test this hypothesis, we injected anti-DβH-SAP saporin at the RVLM and monitored the BP in unanesthetized animals exposed to high salt intake of 2% NaCl solution for 7 days. The injection of anti-DβH-SAP into the RVLM depleted 80% of tyrosine hydroxylase-positive neurons (TH⁺ neurons) in the C1, 38% in the A5, and no significant reduction in the A1 region, when compared to control group (saline as vehicle). High salt intake elicited a significant increase in BP in the control group, while in the anti-DβH-SAP group the depletion of TH⁺ neurons prevents the salt-induced hypertension. Moreover, the low frequency component of systolic BP and pulse interval were increased by high-salt intake in control animals but not in anti-DβH-SAP group, which indirectly suggests that the increase in the BP is mediated by increase in sympathetic activity. In conclusion, our data show that hypertension induced by high-salt intake is dependent on C1 neurons.

高盐摄入能够引起神经内分泌和自主神经反应，包括血管加压素释放和交感神经兴奋，导致动脉血压 (BP) 升高。C1 神经元是位于 RVLM 区域的特定儿茶酚胺能神经元群，它们在稳态失衡下控制血压。因此，在这里我们假设 C1 神经元的消融减轻了高盐摄入引起的高血压。为了验证这一假设，我们在 RVLM 处注射了抗 DβH-SAP 皂草素，并监测了暴露于 2% NaCl 溶液的高盐摄入量 7 天的未麻醉动物的血压。将抗 DβH-SAP 注入 RVLM 耗尽了 80% 的酪氨酸羟化酶阳性神经元 (TH ⁺神经元）在 C1 中，在 A5 中为 38%，与对照组（盐水作为载体）相比，A1 区域没有显着减少。高盐摄入引起对照组的血压显着增加，而在抗 DβH-SAP 组中，TH ⁺神经元的消耗可防止盐引起的高血压。此外，对照动物摄入高盐会增加收缩压和脉搏间隔的低频成分，而抗 DβH-SAP 组则不会，这间接表明血压升高是由交感神经活动增加介导的。总之，我们的数据表明，高盐摄入引起的高血压依赖于 C1 神经元。