Hypertension is a leading cause of cognitive impairment and dementias. Such loss of brain health has a vascular component, but the mechanisms involved are poorly defined. In this issue of the JCI, Koide et al. provide evidence that end-organ effects of hypertension on capillary endothelium and inward-rectifier K+ channels (Kir2.1) impair integrated propagation of electrical signals and vasodilation upstream, resulting in reduced neurovascular coupling (NVC) despite neural activation. NVC was partly restored by amlodipine, but not losartan. Moreover, NVC was improved by eplerenone in the presence of losartan, suggesting a role for aldosterone. These findings support the concept that endothelial cells and Kir2.1 are potential therapeutic targets to prevent or reverse the loss of NVC and the vascular component of cognitive deficits that occur with increased frequency during hypertension.

高血压是认知障碍和痴呆的主要原因。这种大脑健康的损失具有血管成分，但所涉及的机制尚不清楚。在本期 JCI 中，Koide 等人。提供证据表明高血压对毛细血管内皮和内向整流 K+ 通道 (Kir2.1) 的终末器官影响会损害电信号的综合传播和上游血管舒张，导致尽管神经激活，但神经血管耦合 (NVC) 减少。NVC 部分由氨氯地平恢复，但不是氯沙坦。此外，在氯沙坦存在的情况下，依普利酮可改善 NVC，这表明醛固酮的作用。这些发现支持了内皮细胞和Kir2的概念。